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Your search keyword '"Hattersley, Andrew T."' showing total 21 results
Start Over Author "Hattersley, Andrew T." Journal human molecular genetics
21 results on '"Hattersley, Andrew T."'

3. Corrigendum to: A genome-wide association study implicates multiple mechanisms influencing raised urinary albumin–creatinine ratio

Author

Casanova, Francesco, primary, Tyrrell, Jessica, additional, Beaumont, Robin N, additional, Ji, Yingjie, additional, Jones, Samuel E, additional, Hattersley, Andrew T, additional, Weedon, Michael N, additional, Murray, Anna, additional, Shore, Angela C, additional, Frayling, Timothy M, additional, and Wood, Andrew R, additional

Published
2022
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4. Fetal alleles predisposing to metabolically favorable adiposity are associated with higher birth weight

Author

Thompson, William D, primary, Beaumont, Robin N, additional, Kuang, Alan, additional, Warrington, Nicole M, additional, Ji, Yingjie, additional, Tyrrell, Jessica, additional, Wood, Andrew R, additional, Scholtens, Denise M, additional, Knight, Bridget A, additional, Evans, David M, additional, Lowe Jr, William L, additional, Santorelli, Gillian, additional, Azad, Raq, additional, Mason, Dan, additional, Hattersley, Andrew T, additional, Frayling, Timothy M, additional, Yaghootkar, Hanieh, additional, Borges, Maria Carolina, additional, Lawlor, Deborah A, additional, and Freathy, Rachel M, additional

Published
2021
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5. Phenotypic severity of homozygous GCK mutations causing neonatal or childhood-onset diabetes is primarily mediated through effects on protein stability

Author

Raimondo, Anne, Chakera, Ali J., Thomsen, Soren K., Colclough, Kevin, Barrett, Amy, De Franco, Elisa, Chatelas, Alisson, Demirbilek, Huseyin, Akcay, Teoman, Alawneh, Hussein, Flanagan, Sarah E., Van De Bunt, Martijn, Hattersley, Andrew T., Gloyn, Anna L., Ellard, Sian, Abduljabbar, Mohammad A., Al-Zyoud, Mahmoud, Aman, Syed, Bath, Louise, De, Parijat, Deshpande, Neeta, Durmaz, Erdem, Eickmeier, Frank, Elbarbary, Nancy Samir, Fillion, Marc, Jagadeesh, Sujatha M., Kershaw, Melanie, Khan, Waqas I., Mlynarski, Wojciech, Noyes, Kathryn, Peters, Catherine J., Shaw, Nick, Tiron, Irina, Turkkahraman, Doga, Turner, Lesley, Eltonbary, Khadiga Y., and Yuksel, Bilgin

Published
2014
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6. Fetal alleles predisposing to metabolically favorable adiposity are associated with higher birth weight.

Author

Thompson, William D, Beaumont, Robin N, Kuang, Alan, Warrington, Nicole M, Ji, Yingjie, Tyrrell, Jessica, Wood, Andrew R, Scholtens, Denise M, Knight, Bridget A, Evans, David M, Jr, William L Lowe, Santorelli, Gillian, Azad, Raq, Mason, Dan, Hattersley, Andrew T, Frayling, Timothy M, Yaghootkar, Hanieh, Borges, Maria Carolina, Lawlor, Deborah A, and Freathy, Rachel M

Published
2022
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7. Genetic variation in the 15q25 nicotinic acetylcholine receptor gene cluster (CHRNA5–CHRNA3–CHRNB4) interacts with maternal self-reported smoking status during pregnancy to influence birth weight

Author

Tyrrell, Jessica, Huikari, Ville, Christie, Jennifer T., Cavadino, Alana, Bakker, Rachel, Brion, Marie-Jo A., Geller, Frank, Paternoster, Lavinia, Myhre, Ronny, Potter, Catherine, Johnson, Paul C.D., Ebrahim, Shah, Feenstra, Bjarke, Hartikainen, Anna-Liisa, Hattersley, Andrew T., Hofman, Albert, Kaakinen, Marika, Lowe, Lynn P., Magnus, Per, McConnachie, Alex, Melbye, Mads, Ng, Jane W.Y., Nohr, Ellen A., Power, Chris, Ring, Susan M., Sebert, Sylvain P., Sengpiel, Verena, Taal, H. Rob, Watt, Graham C.M., Sattar, Naveed, Relton, Caroline L., Jacobsson, Bo, Frayling, Timothy M., Sørensen, Thorkild I.A., Murray, Jeffrey C., Lawlor, Debbie A., Pennell, Craig E., Jaddoe, Vincent W.V., Hypponen, Elina, Lowe, William L., Jr, Jarvelin, Marjo-Riitta, Davey Smith, George, and Freathy, Rachel M.

Published
2012
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9. Genetic evidence that raised sex hormone binding globulin (SHBG) levels reduce the risk of type 2 diabetes

Author

Perry, John R.B., Weedon, Michael N., Langenberg, Claudia, Jackson, Anne U., Lyssenko, Valeriya, Sparsø, Thomas, Thorleifsson, Gudmar, Grallert, Harald, Ferrucci, Luigi, Maggio, Marcello, Paolisso, Giuseppe, Walker, Mark, Palmer, Colin N.A., Payne, Felicity, Young, Elizabeth, Herder, Christian, Narisu, Narisu, Morken, Mario A., Bonnycastle, Lori L., Owen, Katharine R., Shields, Beverley, Knight, Beatrice, Bennett, Amanda, Groves, Christopher J., Ruokonen, Aimo, Jarvelin, Marjo Riitta, Pearson, Ewan, Pascoe, Laura, Ferrannini, Ele, Bornstein, Stefan R., Stringham, Heather M., Scott, Laura J., Kuusisto, Johanna, Nilsson, Peter, Neptin, Malin, Gjesing, Anette P., Pisinger, Charlotta, Lauritzen, Torsten, Sandbaek, Annelli, Sampson, Mike, Zeggini, MAGIC Ele, Lindgren, Cecilia M., Steinthorsdottir, Valgerdur, Thorsteinsdottir, Unnur, Hansen, Torben, Schwarz, Peter, Illig, Thomas, Laakso, Markku, Stefansson, Kari, Morris, Andrew D., Groop, Leif, Pedersen, Oluf, Boehnke, Michael, Barroso, Inês, Wareham, Nicholas J., Hattersley, Andrew T., McCarthy, Mark I., and Frayling, Timothy M.

Published
2010

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

Author

Gloyn, Anna L., Reimann, Frank, Girard, Christophe, Edghill, Emma L., Proks, Peter, Pearson, Ewan R., Temple, I. Karen, Mackay, Deborah J.G., Shield, Julian P.H., Freedenberg, Debra, Noyes, Kathryn, Ellard, Sian, Ashcroft, Frances M., Gribble, Fiona M., and Hattersley, Andrew T.

Published
2005

16. Meta-analysis of genome-wide association studies for body fat distribution in 694 649 individuals of European ancestry.

Author

Pulit, Sara L, Stoneman, Charli, Morris, Andrew P, Wood, Andrew R, Glastonbury, Craig A, Tyrrell, Jessica, Yengo, Loïc, Ferreira, Teresa, Marouli, Eirini, Ji, Yingjie, Yang, Jian, Jones, Samuel, Beaumont, Robin, Croteau-Chonka, Damien C, Winkler, Thomas W, Consortium, GIANT, Hattersley, Andrew T, Loos, Ruth J F, Hirschhorn, Joel N, and Visscher, Peter M

Published
2019
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17. Genetic evidence that raised sex hormone binding globulin (SHBG) levels reduce the risk of type 2 diabetes

Author

Perry, John R.B., primary, Weedon, Michael N., additional, Langenberg, Claudia, additional, Jackson, Anne U., additional, Lyssenko, Valeriya, additional, Sparsø, Thomas, additional, Thorleifsson, Gudmar, additional, Grallert, Harald, additional, Ferrucci, Luigi, additional, Maggio, Marcello, additional, Paolisso, Giuseppe, additional, Walker, Mark, additional, Palmer, Colin N.A., additional, Payne, Felicity, additional, Young, Elizabeth, additional, Herder, Christian, additional, Narisu, Narisu, additional, Morken, Mario A., additional, Bonnycastle, Lori L., additional, Owen, Katharine R., additional, Shields, Beverley, additional, Knight, Beatrice, additional, Bennett, Amanda, additional, Groves, Christopher J., additional, Ruokonen, Aimo, additional, Jarvelin, Marjo Riitta, additional, Pearson, Ewan, additional, Pascoe, Laura, additional, Ferrannini, Ele, additional, Bornstein, Stefan R., additional, Stringham, Heather M., additional, Scott, Laura J., additional, Kuusisto, Johanna, additional, Nilsson, Peter, additional, Neptin, Malin, additional, Gjesing, Anette P., additional, Pisinger, Charlotta, additional, Lauritzen, Torsten, additional, Sandbaek, Annelli, additional, Sampson, Mike, additional, Zeggini, MAGIC, Ele, additional, Lindgren, Cecilia M., additional, Steinthorsdottir, Valgerdur, additional, Thorsteinsdottir, Unnur, additional, Hansen, Torben, additional, Schwarz, Peter, additional, Illig, Thomas, additional, Laakso, Markku, additional, Stefansson, Kari, additional, Morris, Andrew D., additional, Groop, Leif, additional, Pedersen, Oluf, additional, Boehnke, Michael, additional, Barroso, Inês, additional, Wareham, Nicholas J., additional, Hattersley, Andrew T., additional, McCarthy, Mark I., additional, and Frayling, Timothy M., additional

Published
2009
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18. A distant upstream promoter of the HNF-4 α gene connects the transcription factors involved in maturity-onset diabetes of the young.

Author

Thomas, Heike, Jaschkowitz, Karin, Bulman, Mike, Frayling, Timothy M., Mitchell, Simon M.S., Roosen, Simone, Lingott-Frieg, Anja, Tack, Cees J., Ellard, Sian, Ryffel, Gerhart U., and Hattersley, Andrew T.

Abstract

Maturity-onset diabetes of the young (MODY) is a monogenic, autosomal dominant subtype of early-onset diabetes mellitus due to defective insulin secretion by the pancreatic β -cell in humans. Five different genes have been identified including those encoding the tissue-specific transcription factors expressed in pancreatic β -cells, i.e. HNF-4 α (MODY1), HNF-1 α (MODY3), IPF-1 (also known as PDX-1, MODY4) and HNF-1 β (MODY5). Analyzing the transcription of the HNF-4 α gene, we now identify an alternative promoter, P2, which is 46 kb 5′ to the previously identified P1 promoter of the human gene. Based on RT–PCR this distant upstream P2 promoter represents the major transcription site in pancreatic β -cells, but is also used in hepatic cells. Transfection assays with various deletions and mutants of the P2 promoter reveal functional binding sites for HNF-1α , HNF-1β and IPF-1, the other transcription factors known to encode MODY genes. We demonstrate the significance of this alternative promoter in a large MODY family where a mutated IPF-1 binding site in the P2 promoter of the HNF-4 α gene co-segregates with diabetes (LOD score 3.25). These data suggest a regulatory network of the four MODY transcription factors interconnected at the distant upstream P2 promoter of the HNF-4 α gene. [ABSTRACT FROM AUTHOR]

Published
2001
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19. Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Author

Beaumont, Robin N, Warrington, Nicole M, Cavadino, Alana, Tyrrell, Jessica, Nodzenski, Michael, Horikoshi, Momoko, Geller, Frank, Myhre, Ronny, Richmond, Rebecca C, Paternoster, Lavinia, Bradfield, Jonathan P, Kreiner-Møller, Eskil, Huikari, Ville, Metrustry, Sarah, Lunetta, Kathryn L, Painter, Jodie N, Hottenga, Jouke-Jan, Allard, Catherine, Barton, Sheila J, Espinosa, Ana, Marsh, Julie A, Potter, Catherine, Zhang, Ge, Ang, Wei, Berry, Diane J, Bouchard, Luigi, Das, Shikta, Hakonarson, Hakon, Heikkinen, Jani, Helgeland, Øyvind, Hocher, Berthold, Hofman, Albert, Inskip, Hazel M, Jones, Samuel E, Kogevinas, Manolis, Lind, Penelope A, Marullo, Letizia, Medland, Sarah E, Murray, Anna, Murray, Jeffrey C, Njølstad, Pål R, Nohr, Ellen A, Reichetzeder, Christoph, Ring, Susan M, Ruth, Katherine S, Santa-Marina, Loreto, Scholtens, Denise M, Sebert, Sylvain, Sengpiel, Verena, Tuke, Marcus A, Vaudel, Marc, Weedon, Michael N, Willemsen, Gonneke, Wood, Andrew R, Yaghootkar, Hanieh, Muglia, Louis J, Bartels, Meike, Relton, Caroline L, Pennell, Craig E, Chatzi, Leda, Estivill, Xavier, Holloway, John W, Boomsma, Dorret I, Montgomery, Grant W, Murabito, Joanne M, Spector, Tim D, Power, Christine, Järvelin, Marjo-Ritta, Bisgaard, Hans, Grant, Struan F A, Sørensen, Thorkild I A, Jaddoe, Vincent W, Jacobsson, Bo, Melbye, Mads, McCarthy, Mark I, Hattersley, Andrew T, Hayes, M Geoffrey, Frayling, Timothy M, Hivert, Marie-France, Felix, Janine F, Hyppönen, Elina, Lowe, William L, Evans, David M, Lawlor, Debbie A, Feenstra, Bjarke, and Freathy, Rachel M

Subjects
Genotype, genotype, Gestational Age, Protein Serine-Threonine Kinases, Polymorphism, Single Nucleotide, duration of gestation, Germinal Center Kinases, single nucleotide polymorphism, Birth Weight, Cytochrome P-450 CYP3A, Humans, genetics, Alleles, Adaptor Proteins, Signal Transducing, genome-wide association study, Kv1.3 Potassium Channel, offspring, Receptor, Melatonin, MT2, Association Studies Articles, HMGA2 Protein, Intracellular Signaling Peptides and Proteins, birth weight, Genetic Variation, Proteins, Actins, DNA-Binding Proteins, fetus, mothers, alleles, biobanks, Trans-Activators, Female, Transcription Factor 7-Like 2 Protein, Genome-Wide Association Study
Abstract

Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother–child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P

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20. Genetic variation in the 15q25 nicotinic acetylcholine receptor gene cluster (CHRNA5CHRNA3CHRNB4) interacts with maternal self-reported smoking status during pregnancy to influence birth weight

Author

Ville Huikari, Jessica Tyrrell, Sylvain Sebert, Rachel M. Freathy, Lavinia Paternoster, Marjo-Riitta Järvelin, H. Rob Taal, Catherine Potter, Ellen A. Nohr, Debbie A Lawlor, Alana Cavadino, Mads Melbye, Frank Geller, Susan M. Ring, Rachel Bakker, Caroline L Relton, Marie-Jo Brion, George Davey Smith, Timothy M. Frayling, Andrew T. Hattersley, Verena Sengpiel, Lynn P. Lowe, Graham Watt, Jennifer T. Christie, Bo Jacobsson, Jeffrey C. Murray, Jane W. Y. Ng, Anna-Liisa Hartikainen, Elina Hyppönen, Ronny Myhre, Bjarke Feenstra, Albert Hofman, Vincent W. V. Jaddoe, Thorkild I. A. Sørensen, Alex McConnachie, Craig E. Pennell, Per Magnus, Shah Ebrahim, William L. Lowe, Paul C. D. Johnson, Marika Kaakinen, Chris Power, Naveed Sattar, Epidemiology, Erasmus MC other, Medical Research Council (MRC), Tyrell, Jessica, Huikari, Ville, Christie, Jennifer T, Cavadino, Alana, Bakker, Rachel, Brion, Marie Jo A, Geller, Frank, Paternoster, Lavinia, Myhre, Ronny, Potter, Catherine, Johnson, Paul CD, Ebrahim, Shah, Feenstra, Bjarke, Hartikainen, Anna Liisa, Hattersley, Andrew T, Hofman, Albert, Kaakinen, Marika, Lowe, Lynn P, Magnus, Per, McConnachie, Alex, Melbye, Mads, Ng, Jane WY, Nohr, Ellen A, Power, Chris, Ring, Susan M, Sebert, Sylvain P, Sengpiel, Verena, Taal, H Rob, Watt, Graham CM, Sattar, Naveed, Relton, Caroline L, Jacobsson, Bo, Frayling, Timothy M, Sørensen, Thorkild IA, Murray, Jeffrey C, Lawlor, Debbie A, Pennell, Craig E, Jaddoe, Vincent WV, Hypponen, Elina Tuulikki, Lowe, William L Jr, Jarvelin, Marjo-Riitta, Smith, George Davey, Freathy, Rachel M, and Early Growth Genetics Consortium (EGG)

Subjects
medicine.medical_treatment, VARIANT, Receptors, Nicotinic, 0302 clinical medicine, CHILD, Pregnancy, Birth Weight, 030212 general & internal medicine, 11 Medical and Health Sciences, Genetics (clinical), Genetics & Heredity, RISK, Genetics, 0303 health sciences, education.field_of_study, Obstetrics, CHRNA5, Smoking, Association Studies Articles, WOMEN, General Medicine, 3. Good health, Female, HEALTH, medicine.symptom, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, medicine.medical_specialty, Offspring, Birth weight, Population, Nerve Tissue Proteins, Biology, 03 medical and health sciences, LUNG-CANCER, HYPERGLYCEMIA, Early Growth Genetics (EGG) Consortium, medicine, Humans, Genetic Predisposition to Disease, OUTCOME HAPO, GENOME-WIDE ASSOCIATION, education, Molecular Biology, 030304 developmental biology, Science & Technology, Genetic Variation, Infant, 06 Biological Sciences, medicine.disease, Confidence interval, Low birth weight, COHORT PROFILE, biology.protein, Smoking cessation
Abstract

Maternal smoking during pregnancy is associated with low birth weight. Common variation at rs1051730 is robustly associated with smoking quantity and was recently shown to influence smoking cessation during pregnancy, but its influence on birth weight is not clear. We aimed to investigate the association between this variant and birth weight of term, singleton offspring in a well-powered meta-analysis. We stratified 26 241 European origin study participants by smoking status (women who smoked during pregnancy versus women who did not smoke during pregnancy) and, in each stratum, analysed the association between maternal rs1051730 genotype and offspring birth weight. There was evidence of interaction between genotype and smoking (P 5 0.007). In women who smoked during pregnancy, each additional smoking-related T-allele was associated with a 20 g [95% confidence interval (95% CI): 4-36 g] lower birth weight (P 5 0.014). However, in women who did not smoke during pregnancy, the effect size estimate was 5 g per T-allele (95% CI: 24 to 14 g; P 5 0.268). To conclude, smoking status during pregnancy modifies the association between maternal rs1051730 genotype and offspring birth weight. This strengthens the evidence that smoking during pregnancy is causally related to lower offspring birth weight and suggests that population interventions that effectively reduce smoking in pregnant women would result in a reduced prevalence of low birth weight. © The Author 2012. Published by Oxford University Press. All rights reserved.

Published
2012

21. Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics.

Author

Beaumont RN, Warrington NM, Cavadino A, Tyrrell J, Nodzenski M, Horikoshi M, Geller F, Myhre R, Richmond RC, Paternoster L, Bradfield JP, Kreiner-Møller E, Huikari V, Metrustry S, Lunetta KL, Painter JN, Hottenga JJ, Allard C, Barton SJ, Espinosa A, Marsh JA, Potter C, Zhang G, Ang W, Berry DJ, Bouchard L, Das S, Hakonarson H, Heikkinen J, Helgeland Ø, Hocher B, Hofman A, Inskip HM, Jones SE, Kogevinas M, Lind PA, Marullo L, Medland SE, Murray A, Murray JC, Njølstad PR, Nohr EA, Reichetzeder C, Ring SM, Ruth KS, Santa-Marina L, Scholtens DM, Sebert S, Sengpiel V, Tuke MA, Vaudel M, Weedon MN, Willemsen G, Wood AR, Yaghootkar H, Muglia LJ, Bartels M, Relton CL, Pennell CE, Chatzi L, Estivill X, Holloway JW, Boomsma DI, Montgomery GW, Murabito JM, Spector TD, Power C, Järvelin MR, Bisgaard H, Grant SFA, Sørensen TIA, Jaddoe VW, Jacobsson B, Melbye M, McCarthy MI, Hattersley AT, Hayes MG, Frayling TM, Hivert MF, Felix JF, Hyppönen E, Lowe WL Jr, Evans DM, Lawlor DA, Feenstra B, and Freathy RM

Subjects
Actins genetics, Adaptor Proteins, Signal Transducing, Alleles, Birth Weight physiology, Cytochrome P-450 CYP3A genetics, DNA-Binding Proteins genetics, Female, Genetic Variation genetics, Genotype, Germinal Center Kinases, Gestational Age, HMGA2 Protein genetics, Humans, Intracellular Signaling Peptides and Proteins, Kv1.3 Potassium Channel genetics, Protein Serine-Threonine Kinases genetics, Proteins genetics, Receptor, Melatonin, MT2 genetics, Trans-Activators genetics, Transcription Factor 7-Like 2 Protein genetics, Birth Weight genetics, Genome-Wide Association Study methods, Polymorphism, Single Nucleotide genetics
Abstract

Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P < 5 × 10-8. In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights., (© The Author(s) 2018. Published by Oxford University Press.)

Published
2018
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