Author: "Emma L. Edghill" - Searchworks@Jio Institute Digital Library Search Results

47 results on '"Emma L. Edghill"'

1. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes

Author: Adrian van Rhijn, Emma L. Edghill, Ewan R. Pearson, G. Jan Bruining, Deborah J G Mackay, Jerry Wales, Frances M. Ashcroft, Jennifer F. Antcliff, I. Karen Temple, Javier Aisenberg, Pål R. Njølstad, Shubha Srinivasan, Anna L. Gloyn, Shaun Gorman, Sian Ellard, Timothy M. Frayling, Peter Proks, Zdenek Sumnik, Neville J. Howard, Penelope M. Clark, Julian P.H. Shield, Jose M. C. L Silva, Janne Molnes, Annabelle S. Slingerland, Andrew T. Hattersley, and Pediatrics
Subjects: Male, Heterozygote, medicine.medical_specialty, Developmental Disabilities, medicine.medical_treatment, DNA Mutational Analysis, DEND syndrome, Islets of Langerhans, Diabetes mellitus genetics, Tolbutamide, Neonatal diabetes mellitus, SDG 3 - Good Health and Well-being, Internal medicine, Diabetes Mellitus, medicine, Humans, Potassium Channels, Inwardly Rectifying, Epilepsy, business.industry, Insulin, Infant, Newborn, Sequence Analysis, DNA, General Medicine, Kir6.2, Permanent neonatal diabetes mellitus, medicine.disease, Pedigree, Endocrinology, Transient neonatal diabetes mellitus, Face, Mutation, Female, business, medicine.drug
Abstract: BACKGROUND: Patients with permanent neonatal diabetes usually present within the first three months of life and require insulin treatment. In most, the cause is unknown. Because ATP-sensitive potassium (K(ATP)) channels mediate glucose-stimulated insulin secretion from the pancreatic beta cells, we hypothesized that activating mutations in the gene encoding the Kir6.2 subunit of this channel (KCNJ11) cause neonatal diabetes. METHODS: We sequenced the KCNJ11 gene in 29 patients with permanent neonatal diabetes. The insulin secretory response to intravenous glucagon, glucose, and the sulfonylurea tolbutamide was assessed in patients who had mutations in the gene. RESULTS: Six novel, heterozygous missense mutations were identified in 10 of the 29 patients. In two patients the diabetes was familial, and in eight it arose from a spontaneous mutation. Their neonatal diabetes was characterized by ketoacidosis or marked hyperglycemia and was treated with insulin. Patients did not secrete insulin in response to glucose or glucagon but did secrete insulin in response to tolbutamide. Four of the patients also had severe developmental delay and muscle weakness; three of them also had epilepsy and mild dysmorphic features. When the most common mutation in Kir6.2 was coexpressed with sulfonylurea receptor 1 in Xenopus laevis oocytes, the ability of ATP to block mutant K(ATP) channels was greatly reduced. CONCLUSIONS: Heterozygous activating mutations in the gene encoding Kir6.2 cause permanent neonatal diabetes and may also be associated with developmental delay, muscle weakness, and epilepsy. Identification of the genetic cause of permanent neonatal diabetes may facilitate the treatment of this disease with sulfonylureas.
Published: 2016

2. Mutations in ATP-sensitive K+ channel genes cause transient neonatal diabetes and permanent diabetes in childhood or adulthood

Author: Julian P.H. Shield, Deborah J G Mackay, Sian Ellard, Emma L. Edghill, Karen Temple, Andrew T. Hattersley, Sarah E. Flanagan, David O. Robinson, Ann-Marie Patch, and Anna L. Gloyn
Subjects: endocrine system, medicine.medical_specialty, Potassium Channels, Endocrinology, Diabetes and Metabolism, Birth weight, Receptors, Drug, Gene mutation, Sulfonylurea Receptors, ABCC8, Article, Diabetes mellitus genetics, Neonatal diabetes mellitus, Adenosine Triphosphate, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Diabetes Mellitus, Humans, Potassium Channels, Inwardly Rectifying, biology, business.industry, Infant, Newborn, Infant, Permanent neonatal diabetes mellitus, medicine.disease, Pedigree, Endocrinology, Transient neonatal diabetes mellitus, Child, Preschool, Mutation, biology.protein, ATP-Binding Cassette Transporters, business
Abstract: OBJECTIVE: Transient neonatal diabetes mellitus (TNDM) is diagnosed in the first 6 months of life with remission in infancy or early childhood. For approximately 50% of patients their diabetes will relapse in later life. The majority of cases result from anomalies of the imprinted region on chromosome 6q24 and 14 patients have been reported with K(ATP) channel gene mutations. RESEARCH DESIGN AND METHODS: We determined the 6q24 status in 97 patients with TNDM. In patients where no abnormality was identified the KCNJ11 gene and/or ABCC8 gene which encode the Kir6.2 and SUR1 subunits of the pancreatic beta-cell ATP sensitive potassium (K(ATP)) channel were sequenced. RESULTS: K(ATP) channel mutations were found in 25/97 (26%) TNDM probands (12 KCNJ11, 13 ABCC8) while 69/97 (71%) had chromosome 6q24 abnormalities. The phenotype associated with KCNJ11 and ABCC8 mutations was similar, but markedly different from 6q24 patients who had a lower birth weight, and were diagnosed and remitted earlier (all p
Published: 2016

3. Permanent neonatal diabetes due to paternal germline mosaicism for an activating mutation of the KCNJ11 Gene encoding the Kir6.2 subunit of the beta-cell potassium adenosine triphosphate channel

Author: Sian Ellard, Lorna W. Harries, Rachel R. Scott, Andrew T. Hattersley, Anna L. Gloyn, I. Karen Temple, Elizabeth A. Cummings, Teresa Costa, and Emma L. Edghill
Subjects: Male, Heterozygote, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Mutant, Mutation, Missense, Germline mosaicism, Biology, Arginine, medicine.disease_cause, Biochemistry, Germline, Fathers, Islets of Langerhans, Adenosine Triphosphate, Endocrinology, Germline mutation, Neonatal diabetes mellitus, Internal medicine, Diabetes Mellitus, medicine, Humans, Cysteine, Potassium Channels, Inwardly Rectifying, Gene, Alleles, Germ-Line Mutation, Genetics, Mutation, Mosaicism, Biochemistry (medical), Infant, Newborn, DNA, Kir6.2, medicine.disease, Pedigree, Gene Expression Regulation
Abstract: Activating mutations in the KCNJ11 gene encoding for the Kir6.2 subunit of the beta-cell ATP-sensitive potassium channel have recently been shown to be a common cause of permanent neonatal diabetes. In 80% of probands, these are isolated cases resulting from de novo mutations. We describe a family in which two affected paternal half-siblings were found to be heterozygous for the previously reported R201C mutation. Direct sequencing of leukocyte DNA showed that their clinically unaffected mothers and father were genotypically normal. Quantitative real-time PCR analysis of the father's leukocyte DNA detected no trace of mutant DNA. These results are consistent with the father being a mosaic for the mutation, which is restricted to his germline. This is the first report of germline mosaicism in any form of monogenic diabetes. The high percentage of permanent neonatal diabetes cases due to de novo KCNJ11 mutations suggests that germline mosaicism may be common. The possibility of germline mosaicism should be considered when counseling recurrence risks for the parents of a child with an apparently de novo KCNJ11 activating mutation.
Published: 2016

4. HNF1Bdeletions in patients with young-onset diabetes but no known renal disease

Author: Sian Ellard, Andrew T. Hattersley, Emma L. Edghill, Maggie Shepherd, Richard A. Oram, and Karen Stals
Subjects: Proband, medicine.medical_specialty, Offspring, Endocrinology, Diabetes and Metabolism, 030209 endocrinology & metabolism, Disease, Gastroenterology, law.invention, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, law, Diabetes mellitus, Internal medicine, Internal Medicine, Medicine, Polymerase chain reaction, 030304 developmental biology, Subclinical infection, Cystic kidney, 0303 health sciences, business.industry, medicine.disease, HNF1B, 3. Good health, Cancer research, business
Abstract: Diabet. Med. 30, 114–117 (2013) Abstract Aims Hepatocyte nuclear factor 1β (HNF1B) mutations cause a syndrome of renal cysts and diabetes, with whole gene deletions accounting for approximately 50% of cases. The severity of the renal phenotype is variable, from enlarged cystic kidneys incompatible with life to normal renal development and function. We investigated the prevalence of HNF1B deletions in patients with diabetes but no known renal disease. Methods We tested 461 patients with familial diabetes diagnosed before 45 years, including 258 probands who met clinical criteria for maturity-onset diabetes of the young (two generations affected and at least one family member diagnosed under 25 years). A fluorescent polymerase chain reaction assay was used to analyse two intragenic polymorphic HNF1B markers and identify heterozygous patients who therefore did not have whole gene deletions. Those patients homozygous for both markers were then tested for an HNF1B deletion using multiplex ligation-dependent probe amplification. Results Heterozygous HNF1B intragenic polymorphisms were identified in 337/461 subjects. Multiplex ligation-dependent probe amplification analysis showed an HNF1B gene deletion in three of the remaining 124 probands, all of whom met the criteria for maturity-onset diabetes of the young. Testing of their relatives identified three additional deletion carriers and ultrasound scanning showed renal developmental abnormalities in three of these six patients. Conclusions We estimate that HNF1B mutations account for
Published: 2012
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5. Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11

Author: Emma L. Edghill, Sian Ellard, and Sarah E. Flanagan
Subjects: endocrine system, medicine.medical_specialty, Receptors, Drug, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Sulfonylurea Receptors, medicine.disease_cause, Models, Biological, Infant, Newborn, Diseases, ABCC8, Diabetes mellitus genetics, Endocrinology, KATP Channels, Internal medicine, Diabetes mellitus, Diabetes Mellitus, medicine, Humans, Potassium Channels, Inwardly Rectifying, Genetic Association Studies, Mutation, biology, business.industry, Insulin, Infant, Newborn, medicine.disease, Potassium channel, biology.protein, Sulfonylurea receptor, ATP-Binding Cassette Transporters, Beta cell, business
Abstract: The ATP-sensitive potassium (K(ATP)) channel is composed of two subunits SUR1 and Kir6.2. The channel is key for glucose stimulated insulin release from the pancreatic beta cell. Activating mutations have been identified in the genes encoding these subunits, ABCC8 and KCNJ11, and account for approximately 40% of permanent neonatal diabetes cases. The majority of patients with a K(ATP) mutation present with isolated diabetes however some have presented with the Developmental delay, Epilepsy and Neonatal Diabetes syndrome. This review focuses on mutations in the K(ATP) channel which result in permanent neonatal diabetes, we review the clinical and functional effects as well as the implications for treatment.
Published: 2010
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6. Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis

Author: Jose M. Rial, Lorna W. Harries, Sian Ellard, Kusiel Perlman, Adnan Alshaikh, Khalid Hussain, Zdenek Sumnik, Thiruvengadam Vasanthi, Ildem Akerman, Rüveyde Bundak, Juan M. Fernandez, Guiomar Perez de Nanclares, Dorothee Deiss, Emma L. Edghill, Karen A. Johnstone, Gabriel del Castillo, Jonathan M. Locke, Eduardo Fernandez-Rebollo, Noel G. Morgan, Miguel A. Maestro, Estibaliz Ugarte, Thomasz Klupa, Sarah E. Flanagan, Oscar Rubio-Cabezas, Fauzia Mohsin, Stanislava Kolouskova, Michele O’Connell, Itxaso Rica, Luis Castaño, Asma Deeb, Jorge Ferrer, Carlos Castaño, Klemens Raile, Rosa de Diego Martínez, Intza Garin, Ann-Marie Patch, Koumudi Godbole, and Andrew T. Hattersley
Subjects: Male, Preproinsulin, medicine.medical_treatment, DNA Mutational Analysis, Gene Dosage, Genes, Recessive, 030209 endocrinology & metabolism, Biology, Gene dosage, 03 medical and health sciences, Diabetes mellitus genetics, 0302 clinical medicine, Diabetes mellitus, Diabetes Mellitus, medicine, Humans, Insulin, Protein Precursors, Gene, DNA Primers, 030304 developmental biology, Proinsulin, Regulation of gene expression, Genetics, 0303 health sciences, Multidisciplinary, Infant, Newborn, Biological Sciences, medicine.disease, Mutation, Oligonucleotide Probes
Abstract: Heterozygous coding mutations in the INS gene that encodes preproinsulin were recently shown to be an important cause of permanent neonatal diabetes. These dominantly acting mutations prevent normal folding of proinsulin, which leads to beta-cell death through endoplasmic reticulum stress and apoptosis. We now report 10 different recessive INS mutations in 15 probands with neonatal diabetes. Functional studies showed that recessive mutations resulted in diabetes because of decreased insulin biosynthesis through distinct mechanisms, including gene deletion, lack of the translation initiation signal, and altered mRNA stability because of the disruption of a polyadenylation signal. A subset of recessive mutations caused abnormal INS transcription, including the deletion of the C1 and E1 cis regulatory elements, or three different single base-pair substitutions in a CC dinucleotide sequence located between E1 and A1 elements. In keeping with an earlier and more severe beta-cell defect, patients with recessive INS mutations had a lower birth weight (−3.2 SD score vs. −2.0 SD score) and were diagnosed earlier (median 1 week vs. 10 weeks) compared to those with dominant INS mutations. Mutations in the insulin gene can therefore result in neonatal diabetes as a result of two contrasting pathogenic mechanisms. Moreover, the recessively inherited mutations provide a genetic demonstration of the essential role of multiple sequence elements that regulate the biosynthesis of insulin in man.
Published: 2010
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7. Severe Insulin Resistance and Intrauterine Growth Deficiency Associated With Haploinsufficiency for INSR and CHN2

Author: Emanuela V. Volpi, L Barak, Sian Ellard, Natalie Wilson, Laura J. McCulloch, Daniela Gasperikova, Iwar Klimes, Sara G.I. Suliman, N Misovicova, Emma L. Edghill, Juraj Stanik, Vilja Sandrikova, Anna L. Gloyn, and Katherine S. Elliott
Subjects: Blood Glucose, Male, Receptors, Steroid, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Chromosomal translocation, Compound heterozygosity, Translocation, Genetic, Diabetes mellitus genetics, 0302 clinical medicine, Pregnancy, Insulin, Age of Onset, Growth Disorders, In Situ Hybridization, Fluorescence, Genetics, Regulation of gene expression, 0303 health sciences, Fetal Growth Retardation, Receptors, Thyroid Hormone, biology, C-Peptide, Chromosome Mapping, DNA-Binding Proteins, Female, Haploinsufficiency, Chromosomes, Human, Pair 7, Signal Transduction, Adult, medicine.medical_specialty, 030209 endocrinology & metabolism, 03 medical and health sciences, Insulin resistance, Antigens, CD, Internal medicine, Internal Medicine, medicine, Diabetes Mellitus, Humans, 030304 developmental biology, Sequence Analysis, DNA, medicine.disease, Receptor, Insulin, Insulin receptor, Endocrinology, Gene Expression Regulation, Haplotypes, biology.protein, Insulin Resistance, Chromosomes, Human, Pair 19, Biomarkers
Abstract: OBJECTIVE Digenic causes of human disease are rarely reported. Insulin via its receptor, which is encoded by INSR, plays a key role in both metabolic and growth signaling pathways. Heterozygous INSR mutations are the most common cause of monogenic insulin resistance. However, growth retardation is only reported with homozygous or compound heterozygous mutations. We describe a novel translocation [t(7,19)(p15.2;p13.2)] cosegregating with insulin resistance and pre- and postnatal growth deficiency. Chromosome translocations present a unique opportunity to identify modifying loci; therefore, our objective was to determine the mutational mechanism resulting in this complex phenotype. RESEARCH DESIGN AND METHODS Breakpoint mapping was performed by fluorescence in situ hybridization (FISH) on patient chromosomes. Sequencing and gene expression studies of disrupted and adjacent genes were performed on patient-derived tissues. RESULTS Affected individuals had increased insulin, C-peptide, insulin–to–C-peptide ratio, and adiponectin levels consistent with an insulin receptoropathy. FISH mapping established that the translocation breakpoints disrupt INSR on chromosome 19p15.2 and CHN2 on chromosome 7p13.2. Sequencing demonstrated INSR haploinsufficiency accounting for elevated insulin levels and dysglycemia. CHN2 encoding β-2 chimerin was shown to be expressed in insulin-sensitive tissues, and its disruption was shown to result in decreased gene expression in patient-derived adipose tissue. CONCLUSIONS We present a likely digenic cause of insulin resistance and growth deficiency resulting from the combined heterozygous disruption of INSR and CHN2, implicating CHN2 for the first time as a key element of proximal insulin signaling in vivo.
Published: 2009

8. A genetic syndrome of chronic renal failure with multiple renal cysts and early onset diabetes

Author: Alan H. Stolpen, Christie P. Thomas, Emma L. Edghill, Jerold C. Erlandson, and Andrew T. Hattersley
Subjects: Nephrology, medicine.medical_specialty, Pediatrics, Cardiovascular examination, Kidney cysts, Internal medicine, Diabetes mellitus, medicine, Humans, Family history, Hepatocyte Nuclear Factor 1-beta, business.industry, Syndrome, Kidney Diseases, Cystic, Middle Aged, medicine.disease, Kidney Transplantation, Magnetic Resonance Imaging, Gout, Surgery, Diabetes Mellitus, Type 1, Mutation, Kidney Failure, Chronic, Female, medicine.symptom, business, Multiple renal cysts, Kidney disease
Abstract: Department of Radiology, University of IowaCollege of Medicine, Iowa City, Iowa, USACASE PRESENTATIONThe patient is a 48-year-old female who was referred fora renal transplant evaluation in 2006. She was firstdiagnosed with kidney disease in her teens afterpresenting with fatigue and general malaise. On referral toa local nephrologist approximately 30 years ago, animaging study was performed demonstrating renal cystsand the patient was diagnosed to have medullary cystickidney disease (MCKD). At the age of 19, the patient wasdiagnosed with type 1 diabetes and insulin therapy wasstarted. Over the next several years, her kidney functiondeclined slowly (Figure 1).On presentation for her transplant evaluation, hermajor symptom was fatigue, which had not changedsubstantially in 30 years. She also had occasional backpain, which was attributed to bleeding within renal cysts.The patient had no history of gout or genitourinary tractanomalies.There was no history of kidney disease, gout, ordiabetes in first-degree relatives. She has two healthybrothers and healthy parents and has no children. There isa paternal family history of diabetes in second-degreerelatives. Her first menses was at age 12 and were regularuntil 3 months before her appointment. The patient hashad no pregnancies or miscarriages.Physical examination revealed a temperature of36.91C, pulse 101, and blood pressure of 128/92mmHg.There was no evidence of dysmorphic features,pre-auricular pits, or tophi. Her oropharynx was withoutlesions and her palatal arch and dentition were normal.Fundoscopic examination was significant for evidenceof copper wiring with early AV nicking, scatteredmicroaneurysms without hemorrhage, and sharp diskmargins. Her neck examination showed no goiter orlymphadenopathy. Cardiovascular examination wasnormal and her lung fields were clear to auscultation.Examination of the abdomen was unrevealing with nohepatosplenomegaly. There were no flank masses ortenderness noted.Laboratory studies at the time of transplant evaluationshowed a creatinine of 2.8mg/100 ml with an estimatedglomerular filtration rate of 19.9ml/min/1.73 m
Published: 2008
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9. Insulin Mutation Screening in 1,044 Patients With Diabetes

Author: Maciej T. Malecki, Sian Ellard, Donald F. Steiner, Julie Støy, Andrew Parrish, Louis H. Philipson, Graeme I. Bell, Maggie Shepherd, Ritika R. Kapoor, Sarah E. Flanagan, Chris Boustred, Michael J. MacDonald, Beverley M. Shields, Emma L. Edghill, Khalid Hussain, Andrew T. Hattersley, and Ann-Marie Patch
Subjects: Proband, medicine.medical_specialty, Mutation, Pediatrics, biology, business.industry, Endocrinology, Diabetes and Metabolism, Insulin, medicine.medical_treatment, Gene mutation, Permanent neonatal diabetes mellitus, medicine.disease, medicine.disease_cause, ABCC8, Endocrinology, Neonatal diabetes mellitus, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, biology.protein, business
Abstract: OBJECTIVE— Insulin gene (INS) mutations have recently been described as a cause of permanent neonatal diabetes (PND). We aimed to determine the prevalence, genetics, and clinical phenotype of INS mutations in large cohorts of patients with neonatal diabetes and permanent diabetes diagnosed in infancy, childhood, or adulthood. RESEARCH DESIGN AND METHODS— The INS gene was sequenced in 285 patients with diabetes diagnosed before 2 years of age, 296 probands with maturity-onset diabetes of the young (MODY), and 463 patients with young-onset type 2 diabetes (nonobese, diagnosed RESULTS— We identified heterozygous INS mutations in 33 of 141 probands diagnosed at CONCLUSIONS— We conclude that INS mutations are the second most common cause of PND and a rare cause of MODY. Insulin gene mutation screening is recommended for all diabetic patients diagnosed before 1 year of age.
Published: 2008
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10. Insulin gene mutations as a cause of permanent neonatal diabetes

Author: Siri Atma W. Greeley, Anna Pluzhnikov, Nancy J. Cox, Emma L. Edghill, Julie Støy, Sarah E. Flanagan, Louis H. Philipson, Honggang Ye, Donald F. Steiner, Jennifer E. Below, Andrew T. Hattersley, Veronica Paz, Rebecca B. Lipton, Gregory M. Lipkind, Sian Ellard, Graeme I. Bell, M. Geoffrey Hayes, and Ann-Marie Patch
Subjects: Male, Heterozygote, Protein Folding, medicine.medical_specialty, Preproinsulin, Potassium Channels, Genetic Linkage, Receptors, Drug, medicine.medical_treatment, Molecular Sequence Data, Mutation, Missense, Gene mutation, Biology, Sulfonylurea Receptors, medicine.disease_cause, Models, Biological, Diabetes mellitus genetics, Neonatal diabetes mellitus, Internal medicine, Diabetes Mellitus, medicine, Humans, Insulin, Amino Acid Sequence, Potassium Channels, Inwardly Rectifying, Protein Precursors, Proinsulin, Mutation, Multidisciplinary, Infant, Newborn, Infant, Biological Sciences, Permanent neonatal diabetes mellitus, medicine.disease, Pedigree, Endocrinology, ATP-Binding Cassette Transporters, Female
Abstract: We report 10 heterozygous mutations in the human insulin gene in 16 probands with neonatal diabetes. A combination of linkage and a candidate gene approach in a family with four diabetic members led to the identification of the initial INS gene mutation. The mutations are inherited in an autosomal dominant manner in this and two other small families whereas the mutations in the other 13 patients are de novo . Diabetes presented in probands at a median age of 9 weeks, usually with diabetic ketoacidosis or marked hyperglycemia, was not associated with β cell autoantibodies, and was treated from diagnosis with insulin. The mutations are in critical regions of the preproinsulin molecule, and we predict that they prevent normal folding and progression of proinsulin in the insulin secretory pathway. The abnormally folded proinsulin molecule may induce the unfolded protein response and undergo degradation in the endoplasmic reticulum, leading to severe endoplasmic reticulum stress and potentially β cell death by apoptosis. This process has been described in both the Akita and Munich mouse models that have dominant-acting missense mutations in the Ins2 gene, leading to loss of β cell function and mass. One of the human mutations we report here is identical to that in the Akita mouse. The identification of insulin mutations as a cause of neonatal diabetes will facilitate the diagnosis and possibly, in time, treatment of this disorder.
Published: 2007
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11. Partial and whole gene deletion mutations of the GCK and HNF1A genes in maturity-onset diabetes of the young

Author: Andrew T. Hattersley, Mark W. J. Strachan, Hans Eiberg, T. Hansen, J. Little, Maggie Shepherd, L. Ambye, Lorna W. Harries, J. Cropper, Emma L. Edghill, Sian Ellard, Martina Owens, Oluf Pedersen, Amanda Stride, K. Thomas, and Betül Ersoy
Subjects: Adult, Male, Adolescent, Sequence analysis, Endocrinology, Diabetes and Metabolism, Biology, medicine.disease_cause, Maturity onset diabetes of the young, Glucokinase, Internal Medicine, medicine, Humans, Hepatocyte Nuclear Factor 1-alpha, Age of Onset, Gene, Transcription factor, Genetics, Mutation, medicine.disease, HNF1B, Pedigree, HNF1A, Phenotype, Diabetes Mellitus, Type 2, Child, Preschool, Female, Gene Deletion
Abstract: Heterozygous mutations of glucokinase (GCK) and hepatocyte nuclear factor-1 alpha (HNF1A; also known as hepatic transcription factor 1 [TCF1]) genes are the most common cause of MODY. Genomic deletions of the HNF1B (also known as TCF2) gene have recently been shown to account for one third of mutations causing renal cysts and diabetes syndrome. We investigated the prevalence of partial and whole gene deletions in UK patients meeting clinical criteria for GCK or HNF-1alpha/-4alpha MODY and in whom no mutation had been identified by sequence analysis.A multiplex ligation-dependent probe amplification (MLPA) assay was developed using synthetic oligonucleotide probes for 30 exons of the GCK, HNF1A and HNF4A genes.Partial or whole gene deletions were identified in 1/29 (3.5%) probands using the GCK MLPA assay and 4/60 (6.7%) of probands using the HNF1A/-4A MLPA assay. Four different deletions were detected: GCK exon 2, HNF1A exon 1, HNF1A exons 2 to 10 and HNF1A exons 1 to 10. An additional Danish pedigree with evidence of linkage to HNF1A had a deletion of exons 2 to 10. Testing other family members confirmed co-segregation of the deletion mutations with diabetes in the pedigrees.Large deletions encompassing whole exons can cause GCK or HNF-1alpha MODY and will not be detected by sequencing. Gene dosage assays, such as MLPA, are a useful adjunct to sequence analysis when a diagnosis of MODY is strongly suspected.
Published: 2007
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12. Origin of de Novo KCNJ11 Mutations and Risk of Neonatal Diabetes for Subsequent Siblings

Author: Emma L. Edghill, Julia Rankin, Andrew T. Hattersley, Anna L. Gloyn, Anne Goriely, Lorna W. Harries, Sian Ellard, and Sarah E. Flanagan
Subjects: Adult, Male, Risk, Proband, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Restriction Mapping, Clinical Biochemistry, Pedigree chart, Context (language use), Biology, medicine.disease_cause, Biochemistry, Article, Diabetes mellitus genetics, Endocrinology, Internal medicine, Diabetes Mellitus, medicine, Humans, Potassium Channels, Inwardly Rectifying, Sibling, Allele, Alleles, Germ-Line Mutation, DNA Primers, Genetics, Mutation, Mosaicism, Reverse Transcriptase Polymerase Chain Reaction, Biochemistry (medical), Haplotype, Infant, Newborn, DNA, Pedigree, Haplotypes, Female, Microsatellite Repeats
Abstract: Context: Activating mutations in the KCNJ11 gene, which encodes the Kir6.2 subunit of the pancreatic β-cell KATP channel, result in permanent and transient neonatal diabetes. The majority of KCNJ11 mutations are spontaneous, but the parental origin of these mutations is not known. Objective: Our objective was to determine the parental origin of de novo KCNJ11 mutations and investigate the possibility of mosaicism in transmitting parents. Design: We identified 68 index cases with a KCNJ11 mutation where neither parent was known to be affected. DNA was available from both parents of 41 probands. The parental origin of the mutation was determined in 18 families by examination of pedigrees, microsatellite analysis, or allele-specific PCR. Results: A nonsignificant excess of paternally derived mutations was found with 13 of 18 (72%) shown to have arisen on the paternal allele. There was no evidence to suggest an association with increased age at conception. In two families, there were half-siblings with permanent neonatal diabetes born to an unaffected father, suggesting germline mosaicism that was confirmed by the presence of the R201C mutation in one father’s semen. Somatic mosaicism was detected in one unaffected mother, and this mutation will also be present in her germ cells. Conclusion: De novo KCNJ11 mutations can arise either during gametogenesis or embryogenesis. The possibility of germline mosaicism means that future siblings are at increased risk of neonatal diabetes, and we recommend that molecular genetic testing is routinely offered at birth for subsequent siblings of children with de novo KCNJ11 mutations.
Published: 2007
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13. HLA Genotyping Supports a Nonautoimmune Etiology in Patients Diagnosed With Diabetes Under the Age of 6 Months

Author: Emma L. Edghill, Rachel J. Dix, Polly J. Bingley, Sian Ellard, Andrew T. Hattersley, Sarah E. Flanagan, and Kathleen M Gillespie
Subjects: medicine.medical_specialty, Genotype, Endocrinology, Diabetes and Metabolism, HLA-DQ Antigens, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Genetic predisposition, Humans, Genetic Predisposition to Disease, In patient, Potassium Channels, Inwardly Rectifying, Type 1 diabetes, business.industry, Histocompatibility Antigens Class II, Infant, Newborn, Infant, HLA-DR Antigens, medicine.disease, Control subjects, Diabetes Mellitus, Type 1, Child, Preschool, Immunology, Hla genotyping, Etiology, business
Abstract: Children with permanent diabetes are usually assumed to have type 1 diabetes. It has recently been shown that there are genetic subgroups of diabetes that are often diagnosed during the neonatal period but may present later. A recent Italian study proposed that type 1 diabetes is rare before 6 months of age. We aimed to examine genetic susceptibility to type 1 diabetes in patients diagnosed with diabetes before the age of 2 years. We analyzed HLA class II genotypes, markers of autoimmune diabetes, in 187 children with permanent diabetes diagnosed at
Published: 2006
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14. Mutations in hepatocyte nuclear factor-1 and their related phenotypes

Author: Emma L. Edghill, Sian Ellard, Andrew T. Hattersley, and Coralie Bingham
Subjects: Adult, medicine.medical_specialty, Adolescent, Biology, Gastroenterology, Diabetes mellitus, Internal medicine, Genotype, Genetics, medicine, Humans, Family history, Child, Genetics (clinical), Hepatocyte Nuclear Factor 1-beta, Kidney, Infant, Exons, medicine.disease, Medical Genetics in Practice, Pedigree, Hepatocyte nuclear factors, Phenotype, medicine.anatomical_structure, Endocrinology, Child, Preschool, Mutation, Hepatocyte Nuclear Factor 1-Beta, Medical genetics, Abnormal Liver Function Test, Kidney Diseases
Abstract: Background: Hepatocyte nuclear factor-1 beta (HNF-1β) is a widely distributed transcription factor which plays a critical role in embryonic development of the kidney, pancreas, liver, and Mullerian duct. Thirty HNF-1β mutations have been reported in patients with renal cysts and other renal developmental disorders, young-onset diabetes, pancreatic atrophy, abnormal liver function tests, and genital tract abnormalities. Methods: We sequenced the HNF-1β gene in 160 unrelated subjects with renal disease, 40% of whom had a personal/family history of diabetes. Results: Twenty three different heterozygous HNF-1β mutations were identified in 23/160 subjects (14%), including 10 novel mutations (V61G, V110G, S148L, K156E, Q176X, R276Q, S281fsinsC, R295P, H324fsdelCA, Q470X). Seven (30%) cases were proven to be due to de novo mutations. Renal cysts were found in 19/23 (83%) patients (four with glomerulocystic kidney disease, GCKD) and diabetes in 11/23 (48%, while three other families had a family history of diabetes. Only 26% of families met diagnostic criteria for maturity-onset diabetes of the young (MODY) but 39% had renal cysts and diabetes (RCAD). We found no clear genotype/phenotype relationships. Conclusion: We report the largest series to date of HNF-1β mutations and confirm HNF-1β mutations as an important cause of renal disease. Despite the original description of HNF-1β as a MODY gene, a personal/family history of diabetes is often absent and the most common clinical manifestation is renal cysts. Molecular genetic testing for HNF-1β mutations should be considered in patients with unexplained renal cysts (including GCKD), especially when associated with diabetes, early-onset gout, or uterine abnormalities.
Published: 2005
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15. Insights Into the Pathogenicity of Rare Missense GCK Variants From the Identification and Functional Characterization of Compound Heterozygous and Double Mutations Inherited in Cis

Author: Anna L. Gloyn, Kara Osbak, Jana K. Rundle, Anne Raimondo, Joseph Grimsby, Amy Barrett, Emma L. Edghill, Kirsty J. Wensley, Nicola L. Beer, Kevin Colcough, N. D. Tribble, Martijn van de Bunt, Lucia Valentinova, Anna M. Steele, and Sian Ellard
Subjects: Male, Proband, Heterozygote, Cosegregation, Endocrinology, Diabetes and Metabolism, Mutant, Mutation, Missense, 030209 endocrinology & metabolism, Compound heterozygosity, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Glucokinase, Internal Medicine, medicine, Humans, Missense mutation, Genetic Testing, Original Research, 030304 developmental biology, Genetic testing, Advanced and Specialized Nursing, Genetics, 0303 health sciences, Mutation, medicine.diagnostic_test, business.industry, Clinical Care/Education/Nutrition/Psychosocial Research, Phenotype, Pedigree, Diabetes Mellitus, Type 2, Female, business
Abstract: OBJECTIVE To demonstrate the importance of using a combined genetic and functional approach to correctly interpret a genetic test for monogenic diabetes. RESEARCH DESIGN AND METHODS We identified three probands with a phenotype consistent with maturity-onset diabetes of the young (MODY) subtype GCK-MODY, in whom two potential pathogenic mutations were identified: [R43H/G68D], [E248 K/I225M], or [G261R/D217N]. Allele-specific PCR and cosegregation were used to determine phase. Single and double mutations were kinetically characterized. RESULTS The mutations occurred in cis (double mutants) in two probands and in trans in one proband. Functional studies of all double mutants revealed inactivating kinetics. The previously reported GCK-MODY mutations R43H and G68D were inherited from an affected father and unaffected mother, respectively. Both our functional and genetic studies support R43H as the cause of GCK-MODY and G68D as a neutral rare variant. CONCLUSIONS These data highlight the need for family/functional studies, even for previously reported pathogenic mutations.
Published: 2012
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16. Hypoplastic Glomerulocystic Kidney Disease and Hepatoblastoma

Author: Andrew T. Hattersley, Gregory M. Enns, Andrea Kwan, Emma L. Edghill, and Omar A. Abdul-Rahman
Subjects: Hepatoblastoma, Male, medicine.medical_specialty, Pathology, Internal medicine, Polycystic kidney disease, medicine, Humans, Glomerulocystic kidney disease, Hepatocyte Nuclear Factor 1-beta, Polycystic Kidney Diseases, business.industry, Liver Neoplasms, Infant, Hematology, medicine.disease, Hypoplastic glomerulocystic kidney disease, digestive system diseases, Liver Transplantation, Hepatocyte nuclear factors, Endocrinology, medicine.anatomical_structure, Oncology, Hepatocyte, Mutation, Pediatrics, Perinatology and Child Health, business
Abstract: Hypoplastic glomerulocystic kidney disease is an autosomal dominant disorder caused by mutations in hepatocyte nuclear factor-1beta. Hepatoblastoma is a sporadic occurring tumor of embryonal origin that has been associated with the several overgrowth syndromes. We report a case of concomitant hypoplastic glomerulocystic kidney disease and hepatoblastoma. Review of the literature identified 4 other patients with a similar association. We propose that hypoplastic glomerulocystic kidney disease and hepatoblastoma represent a possible association, and we excluded mutations in hepatocyte nuclear factor-1beta in our patient as causative of this putative association.
Published: 2009
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17. The identification of a R201H mutation in KCNJ11, which encodes Kir6.2, and successful transfer to sustained-release sulphonylurea therapy in a subject with neonatal diabetes: evidence for heterogeneity of beta cell function among carriers of the R201H mutation

Author: Jacek Sieradzki, Andrew T. Hattersley, Maciej T. Malecki, Joanna Nazim, Tomasz Klupa, Emma L. Edghill, and Sian Ellard
Subjects: medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Insulin, medicine.medical_treatment, Kir6.2, Biology, medicine.disease, DEND syndrome, Ketoacidosis, Endocrinology, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Gestation, Beta cell, Glipizide, medicine.drug
Abstract: To the Editor Diabetes caused by severe mutations in beta cell genes is usually diagnosed as neonatal diabetes [1] or MODY [2]. Activating mutations in KCJN11, the gene encoding the ATP-sensitive potassium channel subunit Kir6.2, have been described in very-early-onset diabetes ( A) was found in a single patient. This child was born at 40 weeks’ gestation and weighed 2,450 g. He was diagnosed with diabetes during the third week of life based on a plasma glucose of 35–50 mmol/l, without ketoacidosis, which was measured when he presented with pneumonia and bilateral acute otitis media. The patient was treatedwith insulin, with a dose of 0.7–1.0 U/kg used initially and subsequently decreased. At 9 years, 11 months he weighed 27.5 kg and his daily insulin requirement was 7 U (0.25 U/kg) as a single morning injection of intermediate-acting insulin. Despite little modification to his diet he rarely experienced hyperglycaemia above 11 mmol/l, and had an HbA1c level of 6.6%. These observations suggested endogenous beta cell function, which was confirmed by a fasting plasma C-peptide of 443 pmol/l (glucose 6.7 mmol/l) and an increase in plasma insulin concentration of 70 pmol/l during an IVGTT (Fig. 1). As patients with Kir6.2 diabetes may respond to sulphonylureas, we assessed whether this patient could successfully transfer to sulphonylurea tablets [3, 4]. Glipizide gastrointestinal therapeutic system (GITS), a controlledrelease sulphonylurea, was introduced [5]. A dose of 5 mg was administered for 2 days, then 10 mg; insulin was simultaneously slowly withdrawn over a period of 5 days. As the patient experienced a few mild hypoglycaemic episodes during the first 2 days after the discontinuation of insulin the glipizide GITS dose was decreased to 5 mg. While on this dose, a day profile of his capillary glucose concentrations revealed that they were between 4 and 6 mmol/l; a result confirmed by a 72-h record obtained using a continuous glucose monitoring system (Medtronic, Northridge, CA, USA). The IVGTT was repeated 3 weeks after a stable glipizide dose was achieved. At this time the patient’s fasting glucose level was 5.4mmol/l, and his C-peptide level was 347 pmol/l. T. Klupa and E. L. Edghill contributed equally to this work
Published: 2005
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18. Analysis of transcription factors key for mouse pancreatic development establishes NKX2-2 and MNX1 mutations as causes of neonatal diabetes in man

Author: Sarah E, Flanagan, Elisa, De Franco, Hana, Lango Allen, Michele, Zerah, Majedah M, Abdul-Rasoul, Julie A, Edge, Helen, Stewart, Elham, Alamiri, Khalid, Hussain, Sam, Wallis, Liat, de Vries, Oscar, Rubio-Cabezas, Jayne A L, Houghton, Emma L, Edghill, Ann-Marie, Patch, Sian, Ellard, and Andrew T, Hattersley
Subjects: Homeodomain Proteins, Male, Adolescent, Homozygote, Molecular Sequence Data, Infant, Newborn, Infant, Nuclear Proteins, Zebrafish Proteins, Mice, Homeobox Protein Nkx-2.2, Phenotype, Child, Preschool, Mutation, Diabetes Mellitus, Animals, Humans, Female, Amino Acid Sequence, Pancreas, Transcription Factors
Abstract: Understanding transcriptional regulation of pancreatic development is required to advance current efforts in developing beta cell replacement therapies for patients with diabetes. Current knowledge of key transcriptional regulators has predominantly come from mouse studies, with rare, naturally occurring mutations establishing their relevance in man. This study used a combination of homozygosity analysis and Sanger sequencing in 37 consanguineous patients with permanent neonatal diabetes to search for homozygous mutations in 29 transcription factor genes important for murine pancreatic development. We identified homozygous mutations in 7 different genes in 11 unrelated patients and show that NKX2-2 and MNX1 are etiological genes for neonatal diabetes, thus confirming their key role in development of the human pancreas. The similar phenotype of the patients with recessive mutations and mice with inactivation of a transcription factor gene support there being common steps critical for pancreatic development and validate the use of rodent models for beta cell development.
Published: 2013

19. Heterozygous ABCC8 mutations are a cause of MODY

Author: Andrew T. Hattersley, Annet Damhuis, Sarah E. Flanagan, Maggie Shepherd, Pamela Bowman, Emma L. Edghill, R. Paisey, and Sian Ellard
Subjects: Male, Endocrinology, Diabetes and Metabolism, Receptors, Drug, DNA Mutational Analysis, medicine.disease_cause, Sulfonylurea Receptors, Cohort Studies, 0302 clinical medicine, Leukocytes, Genetics, 0303 health sciences, Mutation, biology, medicine.diagnostic_test, Middle Aged, 3. Good health, HNF1A, Pedigree, Female, hormones, hormone substitutes, and hormone antagonists, Adult, endocrine system, medicine.medical_specialty, Heterozygote, medicine.drug_class, 030209 endocrinology & metabolism, ABCC8, 03 medical and health sciences, Young Adult, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Hypoglycemic Agents, Potassium Channels, Inwardly Rectifying, Genetic Association Studies, 030304 developmental biology, Genetic testing, business.industry, nutritional and metabolic diseases, medicine.disease, Sulfonylurea, United Kingdom, Protein Subunits, Endocrinology, Sulfonylurea Compounds, Amino Acid Substitution, Diabetes Mellitus, Type 2, biology.protein, Congenital hyperinsulinism, Sulfonylurea receptor, ATP-Binding Cassette Transporters, business, Microsatellite Repeats
Abstract: The ABCC8 gene encodes the sulfonylurea receptor 1 (SUR1) subunit of the pancreatic beta cell ATP-sensitive potassium (K(ATP)) channel. Inactivating mutations cause congenital hyperinsulinism (CHI) and activating mutations cause transient neonatal diabetes (TNDM) or permanent neonatal diabetes (PNDM) that can usually be treated with sulfonylureas. Sulfonylurea sensitivity is also a feature of HNF1A and HNF4A MODY, but patients referred for genetic testing with clinical features of these types of diabetes do not always have mutations in the HNF1A/4A genes. Our aim was to establish whether mutations in the ABCC8 gene cause MODY that is responsive to sulfonylurea therapy.We sequenced the ABCC8 gene in 85 patients with a BMI30 kg/m², no family history of neonatal diabetes and who were deemed sensitive to sulfonylureas by the referring clinician or were sulfonylurea-treated. All had tested negative for mutations in the HNF1A and HNF4A genes.ABCC8 mutations were found in seven of the 85 (8%) probands. Four patients were heterozygous for previously reported mutations and four novel mutations, E100K, G214R, Q485R and N1245D, were identified. Only four probands fulfilled MODY criteria, with two diagnosed after 25 years and one patient, who had no family history of diabetes, as a result of a proven de novo mutation.ABCC8 mutations can cause MODY in patients whose clinical features are similar to those with HNF1A/4A MODY. Therefore, sequencing of ABCC8 in addition to the known MODY genes should be considered if such features are present, to facilitate optimal clinical management of these patients.
Published: 2011

20. Sequencing PDX1 (insulin promoter factor 1) in 1788 UK individuals found 5% had a low frequency coding variant, but these variants are not associated with Type 2 diabetes

Author: Andrew T. Hattersley, Mark Walker, Emma L. Edghill, A. Khamis, Katharine R. Owen, Timothy M. Frayling, Graham A. Hitman, Sian Ellard, Mark I. McCarthy, and Michael N. Weedon
Subjects: Male, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, polygenic, Genome-wide association study, Type 2 diabetes, 0302 clinical medicine, Endocrinology, Genotype, genetics, Genetics, variants, 0303 health sciences, education.field_of_study, diabetes, Middle Aged, 3. Good health, Female, Adult, medicine.medical_specialty, Adolescent, Population, 030209 endocrinology & metabolism, Polymorphism, Single Nucleotide, White People, Young Adult, 03 medical and health sciences, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, education, Gene, 030304 developmental biology, Homeodomain Proteins, business.industry, Insulin, Case-control study, Original Articles, Sequence Analysis, DNA, medicine.disease, United Kingdom, Diabetes Mellitus, Type 2, Case-Control Studies, Mutation, Trans-Activators, business, Genome-Wide Association Study
Abstract: AIM: Genome-wide association studies have identified >30 common variants associated with Type 2 diabetes (>5% minor allele frequency). These variants have small effects on individual risk and do not account for a large proportion of the heritable component of the disease. Monogenic forms of diabetes are caused by mutations that occur in 1%. We found no difference in carrier frequency between patients (5.7%) and control subjects (5.0%) (P=0.46). There were also no differences between patients and control subjects when analyses were limited to subsets of variants. The strongest subset were those variants in the DNA binding domain where all five variants identified were only found in patients (P=0.06). CONCLUSION: Approximately 5% of UK individuals carry a PDX1 variant, but there is no evidence that these variants, either individually or cumulatively, predispose to Type 2 diabetes. Further studies will need to consider strategies to assess the role of multiple variants that occur in
Published: 2011

21. Sequencing of candidate genes selected by beta cell experts in monogenic diabetes of unknown aetiology

Author: Emma L, Edghill, Jayne A L, Minton, Christopher J, Groves, Sarah E, Flanagan, Ann-Marie, Patch, Oscar, Rubio-Cabezas, Maggie, Shepherd, Sigurd, Lenzen, Mark I, McCarthy, Sian, Ellard, and Andrew T, Hattersley
Subjects: Adult, Homeodomain Proteins, Male, Adolescent, DNA Mutational Analysis, Nuclear Proteins, Sequence Analysis, DNA, Middle Aged, Polymorphism, Single Nucleotide, Young Adult, Homeobox Protein Nkx-2.2, Gene Frequency, Child, Preschool, Insulin-Secreting Cells, Diabetes Mellitus, Humans, Female, Child, Expert Testimony, Transcription Factors
Abstract: Approximately 39% of cases with permanent neonatal diabetes (PNDM) and about 11% with maturity onset diabetes of the young (MODY) have an unknown genetic aetiology. Many of the known genes causing MODY and PNDM were identified as being critical for beta cell function before their identification as a cause of monogenic diabetes.We used nominations from the EU beta cell consortium EURODIA project partners to guide gene candidacy.Seventeen cases with permanent neonatal diabetes and 8 cases with maturity onset diabetes of the young.The beta cell experts within the EURODIA consortium were asked to nominate 3 "gold", 3 "silver" and 4 "bronze" genes based on biological or genetic grounds. We sequenced twelve candidate genes from the list based on evidence for candidacy.Sequencing ISL1, LMX1A, MAFA, NGN3, NKX2.2, NKX6.1, PAX4, PAX6, SOX2, SREBF1, SYT9 and UCP2 did not identify any pathogenic mutations.Further work is needed to identify novel causes of permanent neonatal diabetes and maturity onset diabetes of the young utilising genetic approaches as well as further candidate genes.
Published: 2010

22. Testing for monogenic diabetes among children and adolescents with antibody-negative clinically defined Type 1 diabetes

Author: Andrew T. Hattersley, Emma L. Edghill, Oscar Rubio-Cabezas, and Jesús Argente
Subjects: Blood Glucose, Male, medicine.medical_specialty, Adolescent, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Gastroenterology, Antibodies, Endocrinology, Internal medicine, Diabetes mellitus, Internal Medicine, Medicine, Humans, Insulin, Child, Pancreatic hormone, Autoantibodies, Glycated Hemoglobin, Type 1 diabetes, business.industry, Autoantibody, Genetic Variation, Infant, medicine.disease, Obesity, HNF1A, Ketoacidosis, Diabetes Mellitus, Type 1, Child, Preschool, Female, business
Abstract: Aims Monogenic diabetes is frequently misdiagnosed as Type 1 diabetes. We aimed to screen for undiagnosed monogenic diabetes in a cohort of children who had a clinical diagnosis of Type 1 diabetes but were pancreatic autoantibody-negative. Methods We studied 252 patients diagnosed clinically with Type 1 diabetes between 6 months and 17 years of age. Pancreatic autoantibodies [islet cell autoantibodies (ICA), glutamic acid decarboxylase antibodies (GADA) and/or insulinoma-associated antigen-2 antibodies (IA2A)] were absent in 25 cases (9.9%). The most frequent genes involved in monogenic diabetes [KCNJ11 and INS for neonatal diabetes and HNF1A and HNF4A for maturity-onset diabetes of the young (MODY)] were directly sequenced. Results Two of the 25 (8%) antibody-negative patients had de novo heterozygous mutations in INS; c.94G>A (G32S) and c.265C>T (R89C). The two patients presented with non-ketotic hyperglycaemia at 8 and 11 months of age. In contrast, the four antibody-positive patients who presented at a similar age (6–12 months) had a more severe metabolic derangement, manifested as ketosis in all four cases, with ketoacidosis in two. At ages 15 and 5 years, both INS mutation patients were prescribed a replacement dose of insulin with good glycaemic control [glycated haemoglobin (HbA1c) 7.0 and 7.2%]. No mutations were found in KCNJ11, HNF1A or HNF4A. Conclusions The identification of patients with monogenic diabetes from children with clinically defined Type 1 diabetes may be helped by clinical criteria including the absence of pancreatic autoantibodies.
Published: 2009

23. Wolcott-Rallison syndrome is the most common genetic cause of permanent neonatal diabetes in consanguineous families

Author: Ian G Jefferson, Amina Balafrej, Oscar Rubio-Cabezas, Angham Al Mutair, Andrew T. Hattersley, Asma Deeb, Ann-Marie Patch, Khalid Hussain, Emma L. Edghill, Jayne A. L. Minton, Sian Ellard, Charles Buchanan, and Sarah E. Flanagan
Subjects: Proband, Male, medicine.medical_specialty, Genotype, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Consanguinity, Compound heterozygosity, Biochemistry, Polymerase Chain Reaction, Congenital Abnormalities, Diabetes mellitus genetics, eIF-2 Kinase, Endocrinology, Diabetes mellitus, Internal medicine, Diabetes Mellitus, Medicine, Humans, Age of Onset, Genetic testing, medicine.diagnostic_test, business.industry, Biochemistry (medical), Homozygote, Gene Amplification, Genetic Diseases, Inborn, Infant, Newborn, DNA, Syndrome, medicine.disease, Liver, Mutation, Female, Original Article, Age of onset, business, Wolcott–Rallison syndrome
Abstract: Mutations in EIF2AK3 cause Wolcott-Rallison syndrome (WRS), a rare recessive disorder characterized by early-onset diabetes, skeletal abnormalities, and liver dysfunction. Although early diagnosis is important for clinical management, genetic testing is generally performed after the full clinical picture develops. We aimed to identify patients with WRS before any other abnormalities apart from diabetes are present and study the overall frequency of WRS among patients with permanent neonatal diabetes.The coding regions of EIF2AK3 were sequenced in 34 probands with infancy-onset diabetes with a clinical phenotype suggestive of WRS (n = 28) or homozygosity at the WRS locus (n = 6).Twenty-five probands (73.5%) were homozygous or compound heterozygous for mutations in EIF2AK3. Twenty of the 26 mutations identified were novel. Whereas a diagnosis of WRS was suspected before genetic testing in 22 probands, three patients with apparently isolated diabetes were diagnosed after identifying a large homozygous region encompassing EIF2AK3. In contrast to nonconsanguineous pedigrees, mutations in EIF2AK3 are the most common known genetic cause of diabetes among patients born to consanguineous parents (24 vs.2%). Age at diabetes onset and birth weight might be used to prioritize genetic testing in the latter group.WRS is the most common cause of permanent neonatal diabetes mellitus in consanguineous pedigrees. In addition to testing patients with a definite clinical diagnosis, EIF2AK3 should be tested in patients with isolated neonatal diabetes diagnosed after 3 wk of age from known consanguineous families, isolated populations, or countries in which inbreeding is frequent.
Published: 2009

24. Mutations in the SLC29A3 gene are not a common cause of isolated autoantibody negative type 1 diabetes

Author: Emma L, Edghill, Shihab, Hameed, Charles F, Verge, Oscar, Rubio-Cabezas, Jesús, Argente, Zdenek, Sumnik, Petra, Dusatkova, Simon T, Cliffe, Raoul C M, Hennekam, Michael F, Buckley, Khalid, Hussain, Sian, Ellard, and Andrew T, Attersley
Subjects: Polymorphism, Genetic, Adolescent, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, DNA Mutational Analysis, Infant, Nucleoside Transport Proteins, Islets of Langerhans, Diabetes Mellitus, Type 1, Gene Frequency, Child, Preschool, Mutation, Humans, Child, Pancreas, Autoantibodies
Published: 2009

25. Mutations in the third gene shown to alter fasting glucose levels in the population (G6PC2) are not a common cause of monogenic forms of pancreatic B-cell dysfunction

Author: Nicola L. Beer, Andrew T. Hattersley, Anna L. Gloyn, P. Fulton, Laura J. McCulloch, and Emma L. Edghill
Subjects: Adult, Blood Glucose, medicine.medical_specialty, Adolescent, G6PC2, Endocrinology, Diabetes and Metabolism, Population, Fasting glucose, Young Adult, Endocrinology, Text mining, Internal medicine, Insulin-Secreting Cells, Internal Medicine, medicine, Humans, Genetic Predisposition to Disease, education, Child, Gene, B cell, education.field_of_study, business.industry, Infant, Pancreatic Diseases, medicine.anatomical_structure, Diabetes Mellitus, Type 1, Child, Preschool, Mutation, Glucose-6-Phosphatase, business
Published: 2009

26. HNF1B mutations associate with hypomagnesemia and renal magnesium wasting

Author: Emma L. Edghill, Adrian S. Woolf, Coralie Bingham, Sarah Ledermann, David A. Long, Detlef Bockenhauer, Lesley Rees, Shazia Adalat, Raoul C.M. Hennekam, Stephen D. Marks, Karen A. Johnstone, Horia Stanescu, Richard S. Trompeter, Harjeeta K. Dhillon, Lorna W. Harries, Sian Ellard, A. Wirsing, William van’t Hoff, Janette Cansick, Paul J.D. Winyard, Rukshana Shroff, Kjell Tullus, Gerhart U. Ryffel, Imran Mushtaq, ANS - Amsterdam Neuroscience, APH - Amsterdam Public Health, and Paediatric Genetics
Subjects: Male, Nephrology, medicine.medical_specialty, Adolescent, Biology, Kidney, Hypocalciuria, Frameshift mutation, Hypomagnesemia, Clinical Research, Internal medicine, medicine, Polycystic kidney disease, Humans, Family, Magnesium, Hepatocyte Nuclear Factor 1-beta, Retrospective Studies, Ultrasonography, Wasting Syndrome, Genetic Carrier Screening, General Medicine, Renal magnesium wasting, medicine.disease, medicine.anatomical_structure, Endocrinology, Mutation, Female, medicine.symptom, Magnesium Deficiency, Glomerular Filtration Rate, Kidney disease
Abstract: Mutations in hepatocyte nuclear factor 1B (HNF1B), which is a transcription factor expressed in tissues including renal epithelia, associate with abnormal renal development. While studying renal phenotypes of children with HNF1B mutations, we identified a teenager who presented with tetany and hypomagnesemia. We retrospectively reviewed radiographic and laboratory data for all patients from a single center who had been screened for an HNF1B mutation. We found heterozygous mutations in 21 (23%) of 91 cases of renal malformation. All mutation carriers had abnormal fetal renal ultrasonography. Plasma magnesium levels were available for 66 patients with chronic kidney disease (stages 1 to 3). Striking, 44% (eight of 18) of mutation carriers had hypomagnesemia (
Published: 2009

27. Permanent neonatal diabetes mellitus due to a C96Y heterozygous mutation in the insulin gene. A case report

Author: Anish, Ahamed, Ambika Gopalakrishnan, Unnikrishnan, Sanket Sharad, Pendsey, Sheela, Nampoothiri, Nisha, Bhavani, Valliyaparambil Pavithran, Praveen, Harish, Kumar, Rohinivilasam Vasukutty, Jayakumar, Vasantha, Nair, Sian, Ellard, and Emma L, Edghill
Subjects: Diagnosis, Differential, Male, Heterozygote, Amino Acid Substitution, Hyperglycemia, Diabetes Mellitus, Humans, Infant, Insulin
Abstract: Neonatal diabetes is a rare disorder with an incidence of 1 in 215,000-500,000 live births with 50% of them having permanent neonatal diabetes mellitus.We present a case of permanent neonatal diabetes mellitus due to a C96Y (c.287GA; p.Cys96Tyr) heterozygous mutation in the insulin (INS) gene. Both the patient and his father (who had childhood-onset insulin-requiring diabetes) were found to be carriers of a heterozygous missense mutation C96Y in exon 3 of the INS gene. It has been hypothesized that these mutations disrupt the folding of the proinsulin molecule and result in a misfolded protein or retention of the protein in the endoplasmic reticulum, resulting in endoplasmic reticulum stress and beta cell apoptosis. Subjects with this form of diabetes will need lifelong insulin therapy.Insulin gene mutations appear to be an important cause of neonatal diabetes worldwide. This is the first report of a case from the Indian subcontinent. It is important to carry out genetic tests for mutations linked to pancreatic beta cell dysfunction in all patients with persistent neonatal diabetes mellitus in order to decide on therapy.
Published: 2008

28. Gene duplications resulting in over expression of glucokinase are not a common cause of hypoglycaemia of infancy in humans

Author: Khalid Hussain, Emma L. Edghill, Martijn van de Bunt, Anna L. Gloyn, and Sian Ellard
Subjects: Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Gene Expression, Gene dosage, Biochemistry, ABCC8, Exon, Endocrinology, Internal medicine, Gene Duplication, Gene duplication, Glucokinase, medicine, Genetics, Humans, Multiplex ligation-dependent probe amplification, Copy-number variation, Child, Gene, Letter to the Editor, Molecular Biology, biology, Infant, Child, Preschool, biology.protein, Congenital Hyperinsulinism, Female
Abstract: It is well established that chromosome rearrangements and duplications which result in the loss of or the over expression of gene(s) can result in syndromes which feature hypoglycaemia [1,2]. More recently studies have demonstrated the importance of “gene dosage” in monogenic disorders of the pancreatic β-cell [3,4]. Investigators routinely screen for mutations using the gold standard methodology of direct sequencing of the coding regions and conserved splice sites of the gene of interest, however this method does not detect heterozygous deletions or duplications of one or more exons of the gene. Hypoglycaemia of infancy (HI) is a rare condition characterised by unregulated insulin secretion despite hypoglycaemia. Mutations in genes encoding the KATP-channel subunits SUR1(ABCC8) and Kir6.2 (KCNJ11), glucokinase (GCK), the mitochondrial enzymes glutamate-dehydrogenase (GLUD1) and short-chain 3-hydroxyacyl-CoA-dehydrogenase (SCHAD) are responsible for approximately 50% of the cases of HI [5]. GCK activating mutations have been reported in a relatively small number of cases (n = 7) of HI and are characterised by regulated insulin secretion albeit at a reduced threshold for glucose stimulated insulin release [6]. The majority of patients can be treated successfully with the potassium channel opener diazoxide or with diet treatment alone, although cases that have undergone partial pancreatectomy have been reported [7]. A number of studies in rodents have shown than over expression of the glucokinase gene results in increased enzyme activity [8–10]. Over expression resulting from GCK gene duplications would result in increased liver and β-cell glucokinase activity and could therefore result in hypoglycaemia. We hypothesised that duplications of GCK might play a role in the pathogenesis of HI and account for the significant number of cases of HI of unknown genetic aetiology. To determine the putative role of partial or whole gene duplications of GCK, we screened the GCK gene for copy number variation using a multiplex ligation-dependent probe amplification (MLPA) assay in unrelated subjects with unexplained HI (n = 33). The clinical characteristics of the patients screened are shown in Table 1. The MLPA assays were performed using a synthetic GCK probe mix as reported by Ellard et al. and the data was analysed as described by Lai et al. [4,11]. No duplications of the GCK gene were detected in the 33 patients screened. Our data therefore suggest that over expression of glucokinase is unlikely to be a common cause of HI in humans but does not exclude rare cases where GCK duplications may contribute to a lowering of blood glucose levels. In conclusion, there is no evidence to support including a GCK dosage assay in the diagnostic testing repertoire for HI. Table 1 Clinical Characteristics of subjects studied
Published: 2008

29. Whole gene deletion of the hepatocyte nuclear factor-1beta gene in a patient with the prune-belly syndrome

Author: Katie Thomas, Emma L. Edghill, Sian Ellard, Christopher J. Mulgrew, Coralie Bingham, and Paul J. Murray
Subjects: Male, Transplantation, Pathology, medicine.medical_specialty, business.industry, Gene deletion, Middle Aged, medicine.disease, Hepatocyte nuclear factors, medicine.anatomical_structure, Nephrology, Prune belly syndrome, Prune belly, Hepatocyte, Cancer research, Medicine, Humans, Prune Belly Syndrome, business, Gene, Transcription factor, Gene Deletion, Kidney disease, Hepatocyte Nuclear Factor 1-beta
Published: 2008

30. Genetic Disorders of the Pancreatic Beta Cell and Diabetes (Permanent Neonatal Diabetes and Maturity-Onset Diabetes of the Young)

Author: Andrew T. Hattersley and Emma L. Edghill
Subjects: biology, business.industry, medicine.disease, Bioinformatics, Phenotype, ABCC8, Maturity onset diabetes of the young, Hepatocyte nuclear factors, Neonatal diabetes mellitus, Diabetes mellitus, biology.protein, Medicine, Beta cell, business, Gene
Abstract: Mutations in critical beta-cell genes can result in monogenic diabetes. This clinically heterogeneous group of disorders usually presents soon after birth as neonatal diabetes, or during childhood or early adulthood as maturity-onset diabetes of the young (MODY). Most defects arise in genes involved in pancreatic beta-cell development or the maintenance of beta-cell function. Studying the phenotype of patients with mutations and the mechanisms by which these mutations result in diabetes gives new insights into normal and pathological functioning of the beta cell. The most common genetic etiology in patients with MODY are mutations in the genes that encode the transcription factors hepatocyte nuclear factor (HNF)-1 alpha (TCF1), HNF-4 alpha (HNF4A) and HNF-1 beta (TCF2), and the glycolytic enzyme glycokinase (GCK). Mutations in each of these genes result in different clinical phenotypes and cause beta-cell dysfunction through different mechanisms. The commonest causes of neonatal diabetes are defects in betacell function, arising from mutations in genes encoding the subunits which form the KATP channel, Kir6.2 (KCNJ11) and SUR1 (ABCC8).
Published: 2008
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31. Low prevalence of mitochondrial DNA 3243AG point mutation in Caucasians with unexplained renal disease

Author: Sian Ellard, Lorna W. Harries, Andrew T. Hattersley, Ravinder J. Singh, Emma L. Edghill, and Coralie Bingham
Subjects: Mitochondrial DNA, Pathology, medicine.medical_specialty, business.industry, Endocrinology, Diabetes and Metabolism, Point mutation, Disease, DNA, Mitochondrial, White People, Endocrinology, Immunology, Internal Medicine, Medicine, Humans, Point Mutation, Diabetic Nephropathies, Kidney Diseases, business
Published: 2007

32. Permanent neonatal diabetes caused by dominant, recessive, or compound heterozygous SUR1 mutations with opposite functional effects

Author: Emma L. Edghill, Andrew T. Hattersley, Sian Ellard, Frances M. Ashcroft, Christophe Girard, Dennis Carson, Sarah E. Flanagan, Lorna W. Harries, Deborah J G Mackay, Julian P.H. Shield, Peter Proks, Ann-Marie Patch, Holger Haberland, Andrew Parrish, Kenju Shimomura, Department of Physiology, Anatomy and Genetics, University of Oxford, and University of Oxford [Oxford]
Subjects: Heterozygote, Potassium Channels, Receptors, Drug, Molecular Sequence Data, 030209 endocrinology & metabolism, Genes, Recessive, Biology, medicine.disease_cause, Compound heterozygosity, Sulfonylurea Receptors, ABCC8, Cohort Studies, 03 medical and health sciences, Diabetes mellitus genetics, 0302 clinical medicine, Neonatal diabetes mellitus, Report, Insulin Secretion, medicine, Genetics, Diabetes Mellitus, Humans, Insulin, Genetics(clinical), Potassium Channels, Inwardly Rectifying, Gene, Genetics (clinical), ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Genes, Dominant, 0303 health sciences, Mutation, Infant, Newborn, Heterozygote advantage, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, medicine.disease, 3. Good health, Pedigree, biology.protein, Sulfonylurea receptor, ATP-Binding Cassette Transporters
Abstract: Heterozygous activating mutations in the KCNJ11 gene encoding the pore-forming Kir6.2 subunit of the pancreatic beta cell K(ATP) channel are the most common cause of permanent neonatal diabetes (PNDM). Patients with PNDM due to a heterozygous activating mutation in the ABCC8 gene encoding the SUR1 regulatory subunit of the K(ATP) channel have recently been reported. We studied a cohort of 59 patients with permanent diabetes who received a diagnosis before 6 mo of age and who did not have a KCNJ11 mutation. ABCC8 gene mutations were identified in 16 of 59 patients and included 8 patients with heterozygous de novo mutations. A recessive mode of inheritance was observed in eight patients with homozygous, mosaic, or compound heterozygous mutations. Functional studies of selected mutations showed a reduced response to ATP consistent with an activating mutation that results in reduced insulin secretion. A novel mutational mechanism was observed in which a heterozygous activating mutation resulted in PNDM only when a second, loss-of-function mutation was also present.
Published: 2006
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33. Autosomal dominant inheritance of non-syndromic renal hypoplasia and dysplasia: dramatic variation in clinical severity in a single kindred

Author: Mushfequr R. Haq, Jonathan Berg, Sue P. A. Rigden, Larissa Kerecuk, Coralie Bingham, Judy Taylor, Emma L. Edghill, Neil J. Sebire, Frances Flinter, Lesley McGregor, Sian Ellard, Adrian S. Woolf, and Anaar Sajoo
Subjects: Adult, Male, Dysplasia, Renal failure, Pathology, medicine.medical_specialty, Adolescent, Nephrogenesis, macromolecular substances, Kidney, Gene, medicine, Humans, Clinical severity, Renal Insufficiency, Child, Family Health, Transplantation, Inheritance, business.industry, Infant, Newborn, Nephrons, Middle Aged, medicine.disease, Renal hypoplasia, Hypoplasia, Pedigree, medicine.anatomical_structure, Nephrology, Child, Preschool, Mutation, Disease Progression, Kidney Failure, Chronic, Female, Kidney Diseases, business, Non syndromic, Kidney disease
Abstract: Autosomal dominant inheritance of non-syndromic renal hypoplasia and dysplasia: dramatic variation in clinical severity in a single kindred.
Published: 2006
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34. KCNJ11 activating mutations are associated with developmental delay, epilepsy and neonatal diabetes syndrome and other neurological features

Author: Régis Coutant, Christine Bellanné-Chantelot, Andrew T. Hattersley, Sylvie Nivot, Sian Ellard, Emma L. Edghill, Catherine Diatloff-Zito, Anna L. Gloyn, and Jean-Jacques Robert
Subjects: Proband, Adult, Male, medicine.medical_specialty, Diabetic neuropathy, Adolescent, Developmental Disabilities, Mutation, Missense, DEND syndrome, Bioinformatics, Epilepsy, Diabetes mellitus, Internal medicine, Genetics, medicine, Diabetes Mellitus, Humans, Potassium Channels, Inwardly Rectifying, Genetics (clinical), business.industry, Infant, Newborn, Muscle weakness, Infant, Exons, Syndrome, medicine.disease, Hypotonia, Introns, Pedigree, Developmental disorder, Endocrinology, Female, medicine.symptom, business
Abstract: Heterozygous activating mutations in the gene encoding for the ATP-sensitive potassium channel subunit Kir6.2 (KCNJ11) have recently been shown to be a common cause of permanent neonatal diabetes. Kir6.2 is expressed in muscle, neuron and brain as well as the pancreatic beta-cell, so patients with KCNJ11 mutations could have a neurological phenotype in addition to their diabetes. It is proposed that some patients with KCNJ11 mutations have neurological features that are part of a discrete neurological syndrome termed developmental Delay, Epilepsy and Neonatal Diabetes (DEND), but there are also neurological consequences of chronic or acute diabetes. We identified KCNJ11 mutations in four of 10 probands with permanent neonatal diabetes and one affected parent; this included the novel C166F mutation and the previously described V59M and R201H. Four of the five patients with mutations had neurological features: the patient with the C166F mutation had marked developmental delay, severe generalised epilepsy, hypotonia and muscle weakness; mild developmental delay was present in the patient with the V59M mutation; one patient with the R201H mutation had acute and chronic neurological consequences of cerebral oedema and another had diabetic neuropathy from chronic hyperglycaemia. In conclusion, the clinical features in these patients support the existence of a discrete neurological syndrome with KCNJ11 mutations. The severe DEND syndrome was seen with the novel C166F mutation and mild developmental delay with the V59M mutation. These features differ markedly from the neurological consequences of acute or chronic diabetes.
Published: 2006

35. Mutations in KCNJ11, which encodes Kir6.2, are a common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype

Author: Emma L. Edghill, Anna L. Gloyn, Sarah E. Flanagan, Andrew T. Hattersley, and Sian Ellard
Subjects: Models, Molecular, endocrine system, medicine.medical_specialty, endocrine system diseases, Genotype, Protein Conformation, Endocrinology, Diabetes and Metabolism, DEND syndrome, Bioinformatics, Global Health, ABCC8, Diabetes mellitus genetics, Genotype-phenotype distinction, Neonatal diabetes mellitus, Internal medicine, Internal Medicine, medicine, Diabetes Mellitus, Humans, Potassium Channels, Inwardly Rectifying, DNA Primers, biology, Base Sequence, Infant, Newborn, nutritional and metabolic diseases, Infant, Kir6.2, Permanent neonatal diabetes mellitus, medicine.disease, Endocrinology, Phenotype, Amino Acid Substitution, Mutation, biology.protein
Abstract: AIMS/HYPOTHESIS: Heterozygous activating mutations in KCNJ11, which encodes the Kir6.2 subunit of the pancreatic ATP-sensitive potassium (K(ATP)) channel, cause both permanent and transient neonatal diabetes. A minority of patients also have neurological features. The identification of a KCNJ11 mutation has important therapeutic implications, as many patients can replace insulin injections with sulfonylurea tablets. We aimed to determine the age of presentation of patients with KCNJ11 mutations and to examine if there was a relationship between genotype and phenotype. SUBJECTS AND METHODS: KCNJ11 was sequenced in 239 unrelated patients from 21 countries, who were diagnosed with permanent diabetes before 2 years of age. RESULTS: Thirty-one of the 120 patients (26%) diagnosed in the first 26 weeks of life had a KCNJ11 mutation; no mutations were found in the 119 cases (0%) diagnosed after this age. Fourteen different heterozygous mutations were identified, with the majority resulting from de novo mutations. These include seven novel mutations: H46Y, R50Q, G53D C166Y, K170T, L164P and Y330S. All 11 probands with the most common mutation, R201H, had isolated diabetes. In contrast, developmental delay in addition to diabetes was seen in four of five probands with the V59M mutation and two of four with the R201C mutation. Five patients with developmental delay, epilepsy and neonatal diabetes (DEND) syndrome had unique mutations not associated with other phenotypes. CONCLUSIONS/INTERPRETATION: KCNJ11 mutations are a common cause of permanent diabetes diagnosed in the first 6 months and all patients diagnosed in this age group should be tested. There is a strong genotype-phenotype relationship with the mutation being an important determinant of associated neurological features.
Published: 2005

36. Relapsing diabetes can result from moderately activating mutations in KCNJ11

Author: Emma L. Edghill, Kathryn Noyes, Debra Freedenberg, Andrew T. Hattersley, Christophe Girard, Fiona M. Gribble, I. Karen Temple, Deborah J G Mackay, Frances M. Ashcroft, Ewan R. Pearson, Julian P.H. Shield, Sian Ellard, Frank Reimann, Peter Proks, and Anna L. Gloyn
Subjects: Adult, Male, Models, Molecular, Proband, Heterozygote, medicine.medical_specialty, Potassium Channels, Receptors, Drug, DNA Mutational Analysis, Biology, Sulfonylurea Receptors, medicine.disease_cause, Inhibitory Concentration 50, Xenopus laevis, Diabetes mellitus genetics, Adenosine Triphosphate, Recurrence, Internal medicine, Diabetes mellitus, Diabetes Mellitus, Genetics, medicine, Animals, Humans, Potassium Channels, Inwardly Rectifying, Molecular Biology, Genetics (clinical), Mutation, Dose-Response Relationship, Drug, Homozygote, Infant, Newborn, Infant, Heterozygote advantage, General Medicine, Permanent neonatal diabetes mellitus, medicine.disease, Phenotype, Pedigree, Rats, Electrophysiology, Endocrinology, Child, Preschool, Oocytes, Sulfonylurea receptor, ATP-Binding Cassette Transporters, Chromosomes, Human, Pair 6, Female
Abstract: Neonatal diabetes can either remit and hence be transient or else may be permanent. These two phenotypes were considered to be genetically distinct. Abnormalities of 6q24 are the commonest cause of transient neonatal diabetes (TNDM). Mutations in KCNJ11, which encodes Kir6.2, the pore-forming subunit of the ATP-sensitive potassium channel (K(ATP)), are the commonest cause of permanent neonatal diabetes (PNDM). In addition to diabetes, some KCNJ11 mutations also result in marked developmental delay and epilepsy. These mutations are more severe on functional characterization. We investigated whether mutations in KCNJ11 could also give rise to TNDM. We identified the three novel heterozygous mutations (G53S, G53R, I182V) in three of 11 probands with clinically defined TNDM, who did not have chromosome 6q24 abnormalities. The mutations co-segregated with diabetes within families and were not found in 100 controls. All probands had insulin-treated diabetes diagnosed in the first 4 months and went into remission by 7-14 months. Functional characterization of the TNDM associated mutations was performed by expressing the mutated Kir6.2 with SUR1 in Xenopus laevis oocytes. All three heterozygous mutations resulted in a reduction in the sensitivity to ATP when compared with wild-type (IC(50) approximately 30 versus approximately 7 microM, P-value for is all
Published: 2005

37. Activating mutations in the KCNJ11 gene encoding the ATP-sensitive K+ channel subunit Kir6.2 are rare in clinically defined type 1 diabetes diagnosed before 2 years

Author: Emma L. Edghill, Andrew T. Hattersley, Peter G. Swift, Edwin A M Gale, Neil T. Raymond, Sian Ellard, Kathleen M Gillespie, Anna L. Gloyn, and A. Paul Lambert
Subjects: Male, medicine.medical_specialty, endocrine system diseases, Endocrinology, Diabetes and Metabolism, medicine.disease_cause, Gastroenterology, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Missense mutation, Humans, Potassium Channels, Inwardly Rectifying, Gene, Mutation, Type 1 diabetes, business.industry, Genome, Human, nutritional and metabolic diseases, Genetic Variation, Kir6.2, medicine.disease, Ketoacidosis, Low birth weight, Endocrinology, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Female, medicine.symptom, business
Abstract: We have recently shown that permanent neonatal diabetes can be caused by activating mutations in KCNJ11 that encode the Kir6.2 subunit of the β-cell ATP-sensitive K+ channel. Some of these patients were diagnosed after 3 months of age and presented with ketoacidosis and marked hyperglycemia, which could have been diagnosed as type 1 diabetes. We hypothesized that KCNJ11 mutations could present clinically as type 1 diabetes. We screened the KCNJ11 gene for mutations in 77 U.K. type 1 diabetic subjects diagnosed under the age of 2 years. One patient was found to be heterozygous for the missense mutation R201C. She had low birth weight, was diagnosed at 5 weeks, and did not have a high risk predisposing HLA genotype. A novel variant, R176C, was identified in one diabetic subject but did not cosegregate with diabetes within the family. In conclusion, we have shown that heterozygous activating mutations in the KCNJ11 gene are a rare cause of clinically defined type 1 diabetes diagnosed before 2 years. Although activating KCNJ11 mutations are rare in patients diagnosed with type 1 diabetes, the identification of a KCNJ11 mutation may have important treatment implications.
Published: 2004

38. Mutations in PTF1A cause pancreatic and cerebellar agenesis

Author: Emma L. Edghill, Graham Goodwin, Peter K. Wellauer, Richard S. Houlston, Karen Barker, Gabrielle S. Sellick, Richard J. Coleman, Christine Garrett, Christina M. Fleischmann, Andrew T. Hattersley, Irene Stolte-Dijkstra, and Anna L. Gloyn
Subjects: Positional cloning, Genetic Linkage, Blotting, Western, Molecular Sequence Data, PROTEIN, Locus (genetics), Biology, Diabetes mellitus genetics, Consanguinity, Mice, Neonatal diabetes mellitus, Genetic linkage, EXOCRINE, Cerebellum, Genetics, medicine, Diabetes Mellitus, Animals, Humans, Pancreas, Cerebellar agenesis, Base Sequence, Chromosomes, Human, Pair 10, Histological Techniques, NEONATAL DIABETES-MELLITUS, Computational Biology, Infant, PTF1-P48, Sequence Analysis, DNA, Permanent neonatal diabetes mellitus, medicine.disease, GENE, Mice, Mutant Strains, Pedigree, medicine.anatomical_structure, Phenotype, SUBUNIT, Mutation, Lod Score, GLUCOKINASE DEFICIENCY, Microsatellite Repeats, Transcription Factors
Abstract: Individuals with permanent neonatal diabetes mellitus usually present within the first three months of life and require insulin treatment(1,2). We recently identified a locus on chromosome 10p13-p12.1 involved in permanent neonatal diabetes mellitus associated with pancreatic and cerebellar agenesis in a genome-wide linkage search of a consanguineous Pakistani family(3). Here we report the further linkage analysis of this family and a second family of Northern European descent segregating an identical phenotype. Positional cloning identified the mutations 705insG and C886T in the gene PTF1A, encoding pancreas transcription factor 1alpha, as disease-causing sequence changes. Both mutations cause truncation of the expressed PTF1A protein C-terminal to the basic-helix-loop-helix domain. Reporter-gene studies using a minimal PTF1A deletion mutant indicate that the deleted region defines a new domain that is crucial for the function of this protein. PTF1A is known to have a role in mammalian pancreatic development(4,5), and the clinical phenotype of the affected individuals implicated the protein as a key regulator of cerebellar neurogenesis. The essential role of PTF1A in normal cerebellar development was confirmed by detailed neuropathological analysis of Ptf1a(-/-) mice.
Published: 2004

39. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

Author: S. Artigas, A V Dreval, Mark I. McCarthy, C Watson, Peter H. Bennett, M Quint, Y Ikeda, E Alpert, F Schiele, H Sekihara, Erik Gylfe, P Lowe, J Kuhlmann, Alain Golay, V Longo, Shahidul Alam Khan Akm., L G Mantovani, M Zawodniak-Szalapska, G Winkler, T Harrity, L Virág, U Johne, Kuo S-W., Linda C Tapsell, J Rodriguez, Michel Komajda, K Kankova, Carole A. Cull, M Sporna, E Estilles, U Ribel, M C Spruce, E Buzzigoli, T Prazak, J K McLaughlin, M K Lingohr, M Lim, F Calara, A Siebenhofer, G Meregalli, Roberto Anichini, A D Baron, R Kurashvili, P C Butler, G I Fantus, T. E. De Gooyer, Park Y-M., R. Walther, S Heinrich, Agnieszka Zawiejska, S Mukherjee, Nikolaos Papanas, G Wong, Ian D. Caterson, David M. Maahs, Shuichi Kaneko, Alexandra E. Butler, Francisco Javier Ampudia-Blasco, O N Kong, Attali J-R., C A Hedman, K Oshinyemi, Nicolle Müller, I C Cranston, N Okumus, M V Vlaiculescu, Balasubramanian Ravikumar, W W Cheatham, K Mukasa, K B Biswas, Annunziata Lapolla, Phil McEwan, G Mader, Gilles Chassot, Dragi Anevski, Werner A. Scherbaum, M Donath, C Hesselmann, R A Gandhi, David E. Moller, Ezio Bonifacio, C Garcia, V Ifandi, P Hornnes, Nieuwenhoven Fav., C Puech, S Pérez-Del-Pulgar, Kim S-R., G Hines, C Rubio Terrés, Michael Gaster, N. Hosszufalusi, A Scholze, Andrew A. Young, Stavros Liatis, F Hariri, S Tan, Paul Valensi, Allan E. Karlsen, J Kim, E. Moberg, J Kaiser, L Berman, G Nelson, A Altkrüger, P Kothare, D B Cook, S Doran, G. van Dijk, Shahnaz Shahinfar, Kim C-S., P Stahl, M Manousaki, S Sigrist, S K Lim, M. P. Stern, A Guberti, C Rezzani, J McKenney, Karl Thomaseth, Sofia Carlsson, M Julia, R Brillante, I Rubesova, T Darkow, E Matsumoto, Wendy M. Macfarlane, M Di Martino, G Bardini, Rossella Menghini, D Duhot, E Farcasiu, Annalisa Natalicchio, I Lindner, J Buvat, Christian L. Brand, Harry Dorchy, Iwona Pietrzak, Z T Luo, P Home, M Ekelund, Jesper Gromada, Kristine Færch, F Piarulli, H Kim, R Mentel, Zsuzsanna K. Zsengellér, Dullaart Rpf., Anton Luger, Thomas A. Pearson, V Manicardi, P Rösen, Feng Y-M., R Morganti, Lars Hansen, Demuth H-U., Haruo Kasai, A Shostak, Rudi Steffensen, G Taylor, Markolf Hanefeld, C Santini, E Hamaguchi, Roberto Miccoli, F Storms, M Cooper, Y Lee, Allison E. Aiello, P Smith, T Suehiro, K Treece, M Waluś, Timothy A Welborn, Simone Baltrusch, E Kontela, S Chai, J Crean, H Yokoyama, Johan G. Eriksson, Rafael Hernández Hernández, J Rodríguez-Saldaña, M P Tornero, G Formoso, D. Lovell, E Bingham, A Mylonakis, M Manteghetti, D Fedele, Antonio Martín-Duce, Ralph A. DeFronzo, D Salcedo, Kurt Højlund, Antonio Petrone, Sheu Whh., C Gutierrez, Flavia Pricci, S Kurita, Z G Abbas, M M Benedetti, Philippe A. Halban, Daniel J. Cox, O Ljungkvist, Justine Davies, J Palsgaard, Lars Sjöström, E Bosi, L Janin-Manificat, W. F. Kelly, M. Fernandez, E Colak, O V Mulyarchik, B Kronshage, F Lang, M Erfurth, Takashi Kadowaki, N Jendrike, U Walter, J Wishart, Y. Neye, D Kim, N Furuhashi, M Barsotti, D Florow, L Ke, L Borgquist, N C Jackson, Ffolliott M. Fisher, V Baskar, K Yoshioka, Bryan A. Wolf, G Chabrier, R Skoumal, Livio Luzi, H Kose, I Pharisien, B. Klein, H Winiarska, M C Johnson, L Griffiths, Nonna Kravchun, C Combe, Baptist Gallwitz, J Zdychova, L Skorda, Jorma Ilonen, W Gao, I N Steen, A Terrinoni, P D Ambery, W Kern, C M Kusminski, Cho M-H., Paolo Pozzilli, Louise G. Grunnet, E Schönle, David R Matthews, Robert W. Taylor, Y Cohen, Kim H-S., M P Eccles, N B Tutuncu, D McDowell, Richard M. Bergenstal, K Takamatsu, T Steiner, Jaan Palgi, Valdemar Grill, N Niculescu, G Federici, S Lehto, P. M. McKeigue, M Barone, Michael E. Trautmann, S Smirnov, J Mannion, M Eto, C Rousseau, M Conti, C S Ernest, Antonio Ceriello, D H Schweitzer, Jung E-D., Andreas Festa, Avijit Lahiri, A Shepelkevich, A Murro, A Kollmann, Jonathan R.S. Arch, R Landgraf, Son H-Y., I Engelsberger, E Agardh, S Rodríguez-Mulero, P J Kraml, K Lee, D. F. Du Toit, E Kim, G Fadini, Williams Ajk., Philip Home, M B Antcieferov, C Perlemoine, D Perrea, Song X-L., D Ruggieri, Krister Bokvist, Heidi Sørensen, Bilbao, G Yoshino, J P Taylor, Shen H-M., S M Furier, R Urquhart, J Wohlgelernter, Jianping Weng, T. Baba, Q Hong, C Silva, Castaigne J-P., M Felaco, X X Zhang, M Jaroň, Milla Rosengård-Bärlund, J G Papp, Toshio Miyata, Lervang H-H., Park M-K., I Kinalska, A Long, Oomen Phn., N Kogawa, Ippolita Patrizia Patera, S. Karadeniz, Dinesh Selvarajah, D S Chung, A Wensaas, Richard Imrich, M Recasens, J Ruxer, O Buchea, E Wilpart, S P Stepanenko, Le Ttd., H Ohgawara, Mariaconsuelo Valentini, A Mondok, M Peltonen, Marianne O. Larsen, K Chatzianagnostou, Agneta Ståhle, A L Ferrari, L Bordier, F Maingrette, A Matsuda, G Vukomanovic, Jakob D. Wikstrom, T Yamakita, E Gorostiaga, J Jin, B Gopalan, Heinz Drexel, S Hewitt, Rury R. Holman, C Dieterle, T L Ruchti, N Asatiani, M Sidira, A Iezzi, A J Sommerfield, D Châtenet, M L Olsen, R Bergemann, C Koehler, T L Kuraeva, B Balas, Christian Berne, E Santos-Mazo, G Smith, A Siejka, R Kožnarová, A Mattina, S Sheikh, A Adomeit, M Rasmussen, J. Fagerudd, N Busciantella Ricci, Nuria Vilarrasa, E Hammar, T L Thoms, L Aydın, Ron G. Rosenfeld, A Nikolajuk, R Gos, C L Morgan, H L Yu, D Dheelchand, S Ramrath, N Boudriga, Jerome I. Rotter, C Jahannault, W M Weston, Folke Lindgärde, M Hertlova, D Knight, A Monroy-Mayorga, E Pardini, A Chamson-Reig, B Franke, Janie McCluskey, Joseph Bryan, C Nikolopoulou, Christie M. Ballantyne, Fausto Santeusanio, L Pegoraro, M Lee, A Klimenko, S Jaiveer, K. Pettersson-Fernholm, Michael A. Nauck, A Ekbom-Schnell, G Deferrari, Riccardo Schiaffini, S. Pampanelli, Khan Aka., David Hopkins, Maija Wessman, M Kamarinos, Noh J-H., O Ebisui, K McCarroll, Jeppe Sturis, Peter Nowotny, N Gorbenko, Åke Sjöholm, David G. Maggs, A E Halseth, B Cresci, A A Ortiz-Gress, A Korakovouni, O Matejkova, C E Mogensen, C J Lin, Ramon Gomis, H Seaman, C Granier, Yang C-H., F Assah, O Sanchez, Fausto Machicao, Peter G. Morris, Alberto Ortiz, A Giardinelli, D Bracaglia, A Gonzalo, S Pavlatos, Andreas Lechner, F Canovic, L Sjolind, Allan Vaag, Birgitte Bruun Nielsen, David A. Ziegler, Vito Lampasona, R Gershoni-Baruch, A. Dei Cas, H Renz, E Mena, Matthew Waltham, Kim D-M., H Levanen, D D Mick, Valentina Alexandrovna Peterkova, E Meskhishvili, Sarah Nutland, R Bustani, John R. Lindsay, M Christoforidou, A Abicht, E Harno, K Cyganek, A Fitchet, S Neelotpol, P Nikishin, P Serradas, J Hinrichsen, M Halvorson, M Chovatia, B Voet, Jinny Willis, E Parretti, M Haslbeck, M Wellard, L Teng, Julio Wainstein, J S Fischer, K. Lalic, D Roggenland, I Gich, R Anwar, Maurizio Cassader, D Serota, X J Li, R J Schotzinger, Vilmundur Gudnason, Björn Zethelius, S A Wootton, W Andrzejewski, R Rezsohazy, R Gao, T Klimentova, T Mazurek, I Bruckner, C Dohrmann, R E James, G daSilva Xavier, Kim S-Y., A Dorca, Stuart J. Pocock, Terri J. Allen, I Giovos, P B Parab, N H Andersen, P Fotinakis, Miriam Cnop, H Lee, Norbert Tennagels, Omorodola I. Abatan, F Ailett, I. Lager, D Manzella, H Hut, Larry A. Distiller, G Lip, Lim S-K., Rong Zhang, T Tsuno, Steen Knudsen, M. Bajardi, Manuel Benito, Dai Sugimoto, Melvin J. Prince, D W Dunstan, D Rankins, K A Majali, G Ozansoy, Isabella Russo, S Uçak, G Annuzzi, R Talar-Wojnarowska, K Lange, S Neugebauer-Baba, Campbell H. Thompson, Eric Renard, P. D. Mountjoy, Z Morrison, Elizabeth A. Davis, Franco Cavallo, C Corvaja, R Antuña, Craig John Currie, H Linnebjerg, He Y-L., A J Palmer, Mariola R. Chacón, H Malinska, M. Jones, R Lichnovská, K Mandes, Paolo Tessari, T Mokhort, A Laina, H. L. Y. Chan, I Schmidt, R Banks, Richard G. IJzerman, L Ksinantova, G Setti, H Vaudry, A Gallo, V Spallone, Chen J-W., Thomas Danne, A Chong, M Hallschmid, S Aczel, S Hulme, N Islam, M Hosoi, P M Ternan, P Di Bartolo, N Bishara, T Shibasaki, Martin A. Osterhoff, Im S-S., M Jecht, T Hamaguchi, S Mattera, K Ways, Elizabeth Northam, U Rajala, Reinhard W. Holl, L Yang, S Panaiotopoulos, K Horvath, R Kluge, Thora B. Bodvarsdottir, Y Dong, Irene Alemanno, C McDougall, Reimar W. Thomsen, M Campbell, W Rabl, John Öhrvik, Yuichiro Yamada, Paola Ungaro, W Benzer, Mike Sampson, Roberto Trevisan, R G Radu, Aas A-M., P E Lobo, Ricardo Scott, S M Son, Josephine M. Forbes, T A Hillier, K L Wyne, Louis L. Nguyen, J Farmer, M H Tan, Kwon H-S., J Yang, L Sandvik, Franco Folli, A K Jenum, M Nguyen, W Pratipanawatr, A L Frederiksen, Rebecca Smith, Lee H-J., A Schäfer, C Manuelli, G S Denver, T Vukovich, B Maceira, K Matsumoto, K. Chokkalingam, Nurcan Üçeyler, P Modi, Timothy M. Morgan, S Mertens, B M Singh, Michaela Riedl, K Iso, C Cucurullo, G. F. Bottazzo, M Calvani, K Hur, J Wetzels, Kazuhiro Takahashi, Y Aso, H Stammer, M G Masding, Fitsum Guebre-Egziabher, J L González-Sánchez, L Armstrong, Alberto Maran, Peter G.F. Swift, S S Popovic, J Starczynski, E Vitacolonna, Luigi Laviola, R W Gelling, Marina Cardellini, D Barilla, Rosa de Diego Martínez, W H Landschulz, Anne Mette Rosenfalck, R K Wong, Kevin E. Schneider, K Peros, Giuseppe Nanni, F Zhang, I Rákóczi, T Iburi, M Nakhjavani, X Q Zhang, S Tournis, Per Lav Madsen, Graham A. Hitman, A. Tura, K Laubner, N D Kostic, Lawrence M. Dolan, R. Sinha Roy, J A Wagner, J. Tuomilehto, J Hauptman, M Abdel-Ghany, D Lacombe, Toralph Ruge, Johannes A Maassen, Triantafyllos Didangelos, K Sasaki, I Argüelles, Klaus Levin, C Popow, Emanuel Christ, R Chetty, L Baillet-Blanco, Jo-Ann Salmon, T Mine, James L. Trevaskis, I Franke, J Gorski, E A Andrianova, A Dayan, A Caballero, Aleksandra Gilis-Januszewska, M Yasujima, Z Kasalová, C.D.A. Stehouwer, F. K. Gorus, G A Nichols, A Glowania, David P. Strachan, P Fredlund, N. F. da Silva, P Reboldi, M Sausbier, K H Groenier, G Stuccio, N Guttman, K R Ahmed, A D Ristic, T Kapellen, J Coutcher, Aldo V. Greco, Oswald Wagner, A Zagayko, Maria Alevizaki, B B Zhang, W F Ferris, Jenny Fredriksson, Lois Jovanovic, J Hänninen, R De Giglio, Kazuo Yagui, O Potterat, P Hamliton, R E Scranton, B Mankovsky, A Stylianou, B Fellström, Abdel-Wahab Yha., M Kitagawa, Katherine L. Baldock, F R Johnson, F Baigts, S D'Addato, F J Sanz, A Mistry, S D Wise, T Pratipanawatr, U R Fölsch, James R.C. 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Chauveau, P, Combe, C, Baillet blanco, L, Beauvieux, M, Gin, H, Heinrich, S, Steiner, T, Ott, U, Holdass, H, Fellström, B, Jardine, A, Staffler, B, Logan, J, Gimpelewicz, C, Stanciu, C, Pena, C, Serafinceanu, C, González posada, J, Hernández, D, Pérez tamajó, L, Ló, A, Herná Alarcó, M, Meneses, M, Barsotti, M, Rizzo, G, Schmauss, S, Havrdova, T, Saudek, F, Boucek, P, Adamec, M, Invitti, C, Gilardini, L, Parati, G, Mazzilli, G, Pontiggia, B, Sartorio, A, Lutgers, H, Groenier, K, Zasadzinska, G, Saryusz wolska, M, Kurktschiev, D, Majdrakova, I, Varbanova, T, Todorova, B, Bajo martinez, A, Bernal, E, Sanchez, O, Ugalde canitrot, A, Sanchez largo, E, Coca robinot, D, Fabregate, R, Calbacho, M, Marquez, J, Saban ruiz, J, Penesova, A, Cizmarova, E, Blazicek, P, De Jongh, R, Serné, E, Ijzerman, R, De Vries, G, Andersen, N, Knudsen, S, Helleberg, K, Mogensen, C, Waluś, M, Idzior waluś, B, Sztefko, K, Cieślik, G, Fedak, D, Wozniakiewicz, E, Lin, S, Guo, M, Lin, C, Liu, X, Francisco, M, Rodriguez rosas, H, Peiró martinez, I, Macías batista, A, Harte, A, Rodriguez cuenca, S, Valsamakis, G, Chetty, R, Anderson, L, Roca, P, Matyka, K, Lasalle, J, Hershon, K, Berman, L, Gibson, E, Gillen, D, Maroni, J, Simmons, D, Hiukka, A, Forder, P, Leinonen, E, Hilden, H, Fruchart, J, Keech, A, Farnier, M, Freeman, M, Macdonell, G, Perevozskaya, I, Mitchel, Y, Gumbiner, B, Didangelos, T, Athyros, V, Mikhailidis, D, Papageorgiou, A, Bouloukos, V, Pehlivanidis, A, Symeonidis, A, Elisaf, M, Mckenney, J, Insull, W, Lewin, A, Maccubbin, D, Kush, D, Schuster, H, Barter, P, Stender, S, Bonnet, J, Morrell, J, Watkins, C, Kallend, D, Stalenhoef, A, Ballantyne, C, Murin, J, Tonstad, S, Rose, H, Wilpshaar, W, Jenkins, A, Karschimkus, C, Dragicevic, G, Rowley, K, Wolthers, T, Best, J, Voet, B, Murdoch, S, Marcovina, S, Brunzell, J, Caparevic, Z, Kostic, N, Ilic, S, Sartore, G, Piarulli, F, Cantaro, S, Reitano, R, Fiore, C, Marin, R, Bassan, S, Manzato, E, Fedele, D, Solini, A, Santini, E, Thornalley, P, Babaei jadidi, R, Karachalias, N, Kupich, C, Ahmed, N, Fowler, A, Baker, A, Starczynski, J, O'Hare, P, Szepietowska, B, Szelachowska, M, Puch, U, Glebocka, A, Quinn, D, Mcternan, C, Bonser, R, Idzior walus, B, Woźniakiewicz, E, Dimitriou, K, Apostolou, O, Kontela, E, Devangelio, E, Gould, E, Serri, O, Roussin, A, Buithieu, J, Mamputu, J, Renier, G, Giordanetti, S, De Amici, E, Poggi, G, Turpini, C, Fratino, P, Garzaniti, A, Banu, I, Paries, J, Roman, G, Negrean, M, Bala, C, Nita, C, Kistorp, C, Gustafsson, F, Chong, A, Lip, G, Galatius, S, Ari, N, Sahilli, M, Ceylan isık, A, Ozansoy, G, Karasu yilmaz, C, Matteucci, E, Rosada, J, Pallini, M, Evangelista, I, Cassetti, G, Giusti, C, Giampietro, O, Capaldo, B, Galderisi, M, Cicala, S, Turco, A, Imbroinise, A, Nosso, G, D'Errico, A, De Divitiis, O, Klimontov, V, Korolyova, E, Jeltova, L, Bondar, I, Tarkun, I, Arslan, B, Canturk, Z, Tarkun, P, Agacdiken, A, Komsuoglu, B, Méneveau, N, Pierre justin, E, Alsayed, M, Sabbah, R, Paulin, S, Marcu, S, Tauveron, I, Zimmermann, C, Schiele, F, Seronde, M, Vautrin, P, Lusson, J, Thieblot, P, Bernard, Y, Mistry, A, Pye, M, Peovska, I, Maksimovic Pavlovic, J, Vavlukis, M, Pop Gorceva, D, Bosevski, M, Scognamiglio, R, Negut, C, De Kreutzenberg, S, Madonna, R, De Caterina, R, Willerson, J, Geng, Y, Vahsen, S, Ledwig, D, Ramrath, S, Frantz, S, Schmidt, I, Calvillo, L, Dienesch, C, Elbing, I, Bischoff, H, Ertl, G, Bauersachs, J, Davydov, A, Mkrtum'Yan, A, Baranova, L, Ikeda, Y, Suehiro, T, Osaki, F, Ota, K, Arii, K, Kumon, Y, Hashimoto, K, Doney, A, Morris, A, Palmer, C, Byun, S, Doo, H, Pagnin, E, Calo, L, Fadini, G, Kubaszek, A, Chai, S, Chai, Q, Rasmussen, L, Ledet, T, Wogensen, L, Lengyel, C, Varró, A, Virág, L, Magyar, J, Bíró, T, Jost, N, Skoumal, R, Nánási, P, Tóth, M, Horkay, F, Papp, J, Zacharopoulou, O, Athanaselis, S, Tsokos, N, Doupis, J, Psallas, M, Cokkinos, D, Pavlatos, S, Liatis, S, Akhobadze, T, Dzneladze, L, Samarguliani, I, Taskiran, M, Rasmussen, V, Jensen, G, Fisher, A, Petrovsky, N, Srikusalanukul, W, Budge, M, Trifunovic zamaklar, D, Zivkovic, M, Jelic, V, Vukomanovic, G, Ristic, A, Seferovic, P, Costa, J, Duarte, S, Manley, S, Sailesh, S, Venkataraman, A, Haider, Y, Groza, I, Oprean, M, Ardelean, A, Morosanu, A, Darkow, T, Vanderplas, A, Mamas, M, Mcelduff, P, Burns, J, Edwards, R, Fitchet, A, Young, R, Gibson, J, Lichiardopol, R, Niculescu, N, Totora, A, Pencea, C, Tomescu, I, Cinteza, M, Manicardi, V, Coscelli, C, Navazio, A, Catellani, E, Michelini, M, Dall'Asta, D, Guberti, A, Piazza, A, Gasparini, E, Pantaleoni, M, Guiducci, U, Manari, A, Sejil, S, Janand delenne, B, Avierinos, J, Habib, G, Labastie, N, Vague, P, Lassmann vague, V, Luźniak, P, Tatoń, J, Wojciechowska Luźniak, A, Zairis, M, Lyras, A, Patsourakos, N, Tsirimbis, V, Foussas, S, Lupón, J, Urrutia, A, Herreros, J, González, B, Coll, R, Altimir, S, Prats, M, Valle, V, Abreu padí, C, Rábago, G, Ivanova, L, Brasacchio, D, Harno, E, Keenan, A, Li, H, Lu, Z, Ke, L, Liu, H, Jeong, I, Chae, M, Choi, M, Yoo, H, Kim, C, Yun, M, Na, M, Kang, Y, Kong, O, Son, S, Kim, I, Tanaka, N, Hosoi, M, Matsuyama, Y, Fukumoto, M, Yamakita, T, Yoshioka, K, Ishii, T, Sato, T, Fujii, S, Aoki, T, Shibata, T, Mizutani, N, Suzuki, J, Fowelin, J, Samuelsson, P, Brandrup wogsen, G, Okumura, K, Tokmakova, A, Staroverova, D, Antcieferov, M, Shutichina, I, Kuntchevich, G, Vriesendorp, T, Morélis, Q, Legemate, D, Schaper, F, Mainas, E, Gkioulmpasanis, I, Panagiotou, I, Vassilikos, G, Skorda, L, Sidira, M, Christoforidou, M, Alaveras, A, Artikis, V, Evdemon, E, Lechleitner, M, Koch, T, Ebenbichler, C, Sturm, W, Moretti, L, Moruzzo, D, Boldrini, E, Pandolfo, C, Kameyama, M, Iwasa, R, Cho, M, Nam, J, Huh, K, Kaplar, M, Paragh, G, Erdei, A, Csongradi, E, Garai, I, Varga, J, Galuska, L, Udvardy, M, Higa, M, Kaneko, Y, Hiroi, N, Koziarska, D, Nowacki, P, Majkowska, L, Luzniak, P, Wojciechowska luźniak, A, Tushuizen, M, Nieuwland, R, Snoeck, D, Sturk, A, Diamant, M, Aguiar, L, Bahia, L, Villela, N, Laflor, C, Conde, C, Bottino, D, Dorigo, D, Bouskela, E, Pu, S, Luo, Z, Lam, K, Dan, Q, Xu, A, Shen, J, Cheng, K, Xu, J, Thamer, C, Stefan, N, Haap, M, Heller, E, Tschritter, O, De Prado, A, Ortiz, A, Ybarra, J, Gich, I, Pou, J, Ehren, M, Roggenland, D, Reinsen, B, Klein, H, Rittig, K, Stock, J, Kocher, B, Balletshofer, B, Shon, H, Chung, D, Nakatani, Y, Matsuhisa, M, Kaneto, H, Hatazaki, M, Yoshiuchi, K, Katakami, N, Kawamori, D, Ohtoshi, K, Sakamoto, K, Matsuoka, T, Ozawa, K, Ogawa, S, Hori, M, Yamasaki, Y, Zitouni, K, Harry, D, Nourooz zadeh, J, Earle, K, Olesen, P, Franco, L, Corvaja, C, Semplicini, A, Ceylan işık, A, Arı, N, Rösen, P, Lee, I, Park, K, Jung, E, Shin, D, Jo, S, Obuobie, K, Prakash, P, Hanna, F, Lazarus, J, Varadhan, L, Gurushankar, J, James, D, Sheikh, S, Gaede, P, Zou, D, Vilarrasa, N, Perez maraver, M, Mena, E, Perez, D, Setti, G, Buckingham, R, Urbančič, V, Stefanovska, A, Bernjak, A, Ažman juvan, K, Kocijančič, A, Glowania, A, Filters, T, Fosmark, D, Torjesen, P, Kilhovd, B, Berg, T, Sandvik, L, Hanssen, K, Mentink, C, Donchenko, G, Stepanenko, S, Maingrette, F, Deng, H, Lindenmair, A, Freudenthaler, A, Baumgartner parzer, S, Nizheradze, K, Khoruzhenko, A, Tronko, N, Sheu, W, Ou, H, Shen, H, Lin, T, Wu, H, Yang, C, Mogylnytska, L, Schmoelzer, I, Davies, J, Band, M, Struthers, A, Prázný, M, Škrha, J, Kasalová, Z, Neelotpol, S, Jahan, P, Kauschke, S, Harrop, C, Schäfer, A, Widder, J, Eigenthaler, M, Walter, U, Uchimura, I, Ikebukuro, M, Kaibara, M, Hirata, M, Helal, R, Pervin, F, Yang, X, Jansson, P, Nagaev, I, Jack, M, Carvalho, E, Sunnerhagen, K, Cam, M, Cushman, S, Smith, U, Creely, S, Farmer, J, Gustafson, B, Kusminski, C, Krusinova, E, Wohl, P, Klementova, M, Lanska, V, Mcdougall, C, Kelly, I, Abbas, Z, Lutale, J, Archibald, L, Karunajeewa, H, Stingemore, N, Stuccio, G, Mcgechie, D, Muller, L, Hak, E, Goudzwaard, W, Montorsi, F, Homering, M, Sprenger, K, Goldstein, I, Asnaghi, V, Ferrari, G, Rastaldi, M, Gabellini, D, Dell'Antonio, G, Maestroni, A, Ruggieri, D, Luzi, L, Piemonti, L, Zerbini, G, Anafaroglu, I, Tutuncu, N, Sultana, M, Siddiqua, N, Iwasaki, T, Nakajima, A, Yoneda, M, Mukasa, K, Tanaka, S, and Sekihara, H
Subjects: 0303 health sciences, medicine.medical_specialty, business.industry, EASD, Endocrinology, Diabetes and Metabolism, Human physiology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Diabetes mellitus, Family medicine, Internal Medicine, Medicine, business, 030217 neurology & neurosurgery, 030304 developmental biology
Published: 2004

40. RET gene mutations are not a common cause of congenital solitary functioning kidney in adults

Author: Adrian S. Woolf, Sian Ellard, Emma L. Edghill, Raoul C.M. Hennekam, Andrew T. Hattersley, Richard A. Oram, and Coralie Bingham
Subjects: Transplantation, Pathology, medicine.medical_specialty, endocrine system diseases, biology, business.industry, Context (language use), Multiple endocrine neoplasia type 2, medicine.disease, Null allele, Bilateral Renal Agenesis, Nephrology, Dysplasia, Ureteric bud, medicine, Glial cell line-derived neurotrophic factor, biology.protein, Letters, business, Renal agenesis
Abstract: Sir, RET (rearranged during transfection) is a transmembrane receptor tyrosine kinase. Loss-of-function RET mutations occur in Hirschsprung disease, while gain-of-function mutations cause multiple endocrine neoplasia type 2 (MEN2) and familial medullary thyroid carcinoma (FMTC) [1]. In mice, Ret initiates mouse kidney development by enhancing ureteric bud outgrowth [2]. Renal agenesis occurs in mice with homozygous null mutation of either Ret, Gdnf or Gfra1, the latter two genes, respectively, coding for a key ligand that activates Ret and a Ret co-receptor [2]. In humans, unilateral renal agenesis occurs in around 0.01% births and results in a solitary functioning kidney, whereas bilateral renal agenesis and/or severe dysplasia occurs in a similar frequency and usually leads to neonatal death [3]. A role for RET in human kidney development was suggested by a report of unilateral renal agenesis in two members of a FMTC family with RET mutation [4]. More recently, RET mutations were reported in 7 of 19 fetuses with bilateral renal agenesis, and in 2 of 10 with unilateral agenesis and contralateral dysplasia [5]. However, the prevalence of RET mutations in adults with congenital solitary functioning kidney is unknown. A cohort of 14 subjects were selected for our current study. They were living adults born with a solitary functioning kidney, one of whom had two failed pregnancies with fetuses affected by malformed kidneys. We screened exons 1–20 and the conserved splice-sites of RET using direct sequencing. None of the cohort were known to have Hirschsprung disease or MEN2/FMTC or other recognized genetic syndrome. We did not identify any mutations in the 14 adults, and thus it is unlikely that RET mutations will be a common cause of solitary functioning kidney in adults. Because mutations of hepatocyte nuclear factor 1B have been reported in the context of solitary functioning kidney [6], we also screened this gene by sequencing and by dosage analysis but failed to find mutations. Other genes such as GDNF and GFRA1 have yet to be elucidated in our cohort. Our study was in adults while Skinner et al. [5] studied fetuses. We therefore suggest that human RET mutations causing renal disease lead to severe renal failure incompatible with postnatal survival. Mutations of nephrogenesis genes other than RET should be sought to explain human congenital solitary functioning kidney. Conflict of interest statement. None declared.
Published: 2009

41. Mutations in the hepatocyte nuclear factor-1β (HNF1B) gene are common with combined uterine and renal malformations but are not found with isolated uterine malformations

Author: Ida Ismail-Pratt, Richard A. Oram, Coralie Bingham, Sian Ellard, Emma L. Edghill, Miles J.O. Taylor, Sarah E. Flanagan, Tracey Kay, Andrew T. Hattersley, Jenny Blackman, and Sarah M. Creighton
Subjects: Proband, Pathology, medicine.medical_specialty, Uterus, Kidney, medicine.disease_cause, Polymerase Chain Reaction, Cohort Studies, medicine, Humans, Hepatocyte Nuclear Factor 1-beta, Mutation, business.industry, Obstetrics and Gynecology, Sequence Analysis, DNA, HNF1B, HNF1B Gene, medicine.disease, Hepatocyte nuclear factors, medicine.anatomical_structure, Dysplasia, Hepatocyte Nuclear Factor 1-Beta, Female, business, Gene Deletion
Abstract: Objective Congenital uterine abnormalities are common and may be associated with developmental renal abnormalities. Mutations of the hepatocyte nuclear factor-1β ( HNF1B) gene are associated with renal and uterine abnormalities. We aimed to study the role of HNF1B mutations in a cohort with congenital uterine abnormalities. Study Design We tested 108 probands with uterine abnormalities for HNF1B mutations. We collected clinical information from patient records. Results Nine of 108 women (8%) had a mutation or deletion in the HNF1B gene. Abnormal HNF1B was found in 18% of the 50 probands who had both uterine and renal abnormalities but in none of the 58 women with isolated uterine abnormalities. Conclusion Mutations of the HNF1B gene are found in women with both uterine and renal abnormalities but are rare in isolated uterine abnormalities. We suggest that HNF1B testing should be performed in patients with both renal and uterine abnormalities, but not in patients with isolated uterine abnormalities.
Published: 2010
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42. Erratum

Author: Andrew T. Hattersley, Sarah E. Flanagan, Julian P.H. Shield, Karen Temple, Emma L. Edghill, Deborah J G Mackay, David O. Robinson, Ann-Marie Patch, Anna L. Gloyn, and Sian Ellard
Subjects: medicine.medical_specialty, Endocrinology, Neonatal diabetes, business.industry, Endocrinology, Diabetes and Metabolism, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Atp sensitive k channel, medicine.disease, business, Gene
Published: 2008
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43. Autosomal dominant inheritance of non-syndromic renal hypoplasia and dysplasia: dramatic variation in clinical severity in a single kindred.

Author: Larissa Kerecuk, Anaar Sajoo, Lesley McGregor, Jonathan Berg, Mushfequr R. Haq, Neil J. Sebire, Coralie Bingham, Emma L. Edghill, Sian Ellard, Judy Taylor, Sue Rigden, Frances A. Flinter, and Adrian S. Woolf
Published: 2007

44. Transcription factor HNF1β and novel partners affect nephrogenesis

Author: Coralie Bingham, Sian Ellard, Emma L. Edghill, Nima Mottalebi, Sabine Senkel, Stefan Rosengarten, Magdalena Roose, Karin Dudziak, and Gerhart U. Ryffel
Subjects: Transcriptional Activation, Embryo, Nonmammalian, Organogenesis, Ubiquitin-Protein Ligases, Xenopus, DNA Mutational Analysis, Kidney development, Biology, Kidney, Maturity onset diabetes of the young, Transactivation, Two-Hybrid System Techniques, medicine, Animals, Humans, Transcription factor, transcription factor, Hepatocyte Nuclear Factor 1-beta, kidney development, Genetics, Gene Expression Regulation, Developmental, genetic renal disease, medicine.disease, Pronephros, Cell biology, Repressor Proteins, Hepatocyte nuclear factors, HNF1β, medicine.anatomical_structure, Nephrology, Pronephros formation, Butyrate Response Factor 1
Abstract: Heterozygous mutations of the tissue-specific transcription factor hepatocyte nuclear factor (HNF)1beta, cause maturity onset diabetes of the young (MODY5) and kidney anomalies including agenesis, hypoplasia, dysplasia and cysts. Because of these renal anomalies, HNF1beta is classified as a CAKUT (congenital anomalies of the kidney and urinary tract) gene. We searched for human fetal kidney proteins interacting with the N-terminal region of HNF1beta using a bacterial two-hybrid system and identified five novel proteins along with the known partner DCoH. The interactions were confirmed for four of these proteins by GST pull-down assays. Overexpression of two proteins, E4F1 and ZFP36L1, in Xenopus embryos interfered with pronephros formation. Further, in situ hybridization showed overlapping expression of HNF1beta, E4F1 and ZFP36L1 in the developing pronephros. HNF1beta is present largely in the nucleus where it colocalized with E4F1. However, ZFP36L1 was located predominantly in the cytoplasm. A nuclear function for ZFP36L1 was shown as it was able to reduce HNF1beta transactivation in a luciferase reporter system. Our studies show novel proteins may cooperate with HNF1beta in human metanephric development and propose that E4F1 and ZFP36L1 are CAKUT genes. We searched for mutations in the open reading frame of the ZFP36L1 gene in 58 patients with renal anomalies but found none.
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45. Renal cysts and diabetes due to a heterozygous HNF-1β gene deletion.

Author: Philipp Eller, Susanne Kaser, Karl Lhotta, Emma L. Edghill, Sian Ellard, Christoph Ebenbichler, and Josef R. Patsch
Published: 2007
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46. Whole gene deletion of the hepatocyte nuclear factor-1{beta} gene in a patient with the prune-belly syndrome.

Author: Paul J. Murray, Katie Thomas, Christopher J. Mulgrew, Sian Ellard, Emma L. Edghill, and Coralie Bingham
Published: 2008
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47. Hepatocyte nuclear factor-1{beta} gene deletions--a common cause of renal disease.

Author: Emma L. Edghill, Richard A. Oram, Martina Owens, Karen L. Stals, Lorna W. Harries, Andrew T. Hattersley, Sian Ellard, and Coralie Bingham
Subjects: *KIDNEY diseases, *ENDOCRINE diseases, *DIABETES, *CYSTS (Pathology)
Abstract: Background. Hepatocyte nuclear factor-1β (HNF-1β) is a critical transcription factor in pancreatic and renal development. Our previous report identified HNF-1β mutations in 23/160 patients with unexplained renal disease. The most common phenotype is renal cysts, which is frequently associated with early-onset diabetes in the renal cysts and diabetes (RCAD) syndrome. HNF-1β gene deletions have recently been shown to cause renal malformations and early-onset diabetes. Methods. We developed a multiplex ligation-dependent probe amplification (MLPA) assay for HNF-1β gene dosage analysis and tested patients with unexplained renal disease in whom mutations had not been found by sequencing. Results. Whole HNF-1β gene deletions were detected in 15/133 probands. Renal cysts were present in 13/15, including three with glomerulocystic kidney disease and one with cystic renal dysplasia. Renal function ranged from normal to transplantation aged 3 years. Ten probands had diabetes (nine having RCAD). In addition, four had abnormal liver function tests, two showed pancreatic atrophy and 3/10 female probands had uterine malformations. Whole HNF-1β gene deletions are a common cause of developmental renal disease, particularly renal cystic disease with or without diabetes. Conclusions. The phenotype associated with deletions or coding region/splicing mutations is very similar suggesting that haploinsufficiency is the underlying mechanism. Patients with features suggestive of the HNF-1β clinical phenotype should be tested for mutations both by sequence and dosage analysis. [ABSTRACT FROM AUTHOR]
Published: 2008

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