43 results on '"Johansson, Bente B."'
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2. In Vitro Functional Analysis Can Aid Precision Diagnostics of HNF1B-MODY
3. Author Correction: Characterization of the genetic architecture of infant and early childhood body mass index
4. Characterization of the genetic architecture of infant and early childhood body mass index
5. Abnormal exocrine–endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8
6. Common single-base insertions in the VNTR of the carboxyl ester lipase (CEL) gene are benign and also likely to arise somatically in the exocrine pancreas
7. Characterization of CEL-DUP2: Complete duplication of the carboxyl ester lipase gene is unlikely to influence risk of chronic pancreatitis
8. The role of the carboxyl ester lipase (CEL) gene in pancreatic disease
9. Protein misfolding in combination with other risk factors in CEL-HYB1-mediated chronic pancreatitis
10. Copy number variants and VNTR length polymorphisms of the carboxyl-ester lipase (CEL) gene as risk factors in pancreatic cancer
11. The genetic risk factor CEL-HYB1 causes proteotoxicity and chronic pancreatitis in mice
12. Targeted next-generation sequencing reveals MODY in up to 6.5% of antibody-negative diabetes cases listed in the Norwegian Childhood Diabetes Registry
13. Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases
14. Glycogenin-2 Is Dispensable for Liver Glycogen Synthesis and Glucagon-Stimulated Glucose Release
15. Characterization of the genetic architecture of BMI in infancy and early childhood reveals age-specific effects and implicates pathways involved in Mendelian obesity
16. The position of single-base deletions in the VNTR sequence of the carboxyl ester lipase (CEL) gene determines proteotoxicity
17. The position of single-base deletions in the VNTR sequence of the carboxyl ester lipase (CEL) gene determines pathogenicity
18. Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases.
19. Gα12 binds to the N-terminal regulatory domain of p120ctn, and downregulates p120ctn tyrosine phosphorylation induced by Src family kinases via a RhoA independent mechanism
20. 1638-P: Functional Characterization of HNF1B Variants Can Enhance Diabetes Precision Medicine
21. 83-OR: Pancreatic Exocrine to Endocrine Cell Cross Talk Mediates Endoplasmic Reticulum Stress and Beta-Cell Dysfunction in MODY8
22. Pathogenic Carboxyl Ester Lipase (CEL) Variants Interact with the Normal CEL Protein in Pancreatic Cells
23. Proteasome involvement in the degradation of the Gq family of Gα subunits
24. Two New Mutations in the CELGene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases
25. Protein misfolding in combination with other risk factors in CEL-HYB1-mediated chronic pancreatitis.
26. The mucinous domain of pancreatic carboxyl-ester lipase (CEL) contains core 1/core 2 O-glycans that can be modified by ABO blood group determinants
27. Altered O- and N-linked glycosylation profiles in carboxyl ester lipase (CEL) protein variants involved in chronic pancreatitis and MODY8 syndrome
28. The polymorphic carboxyl-ester lipase (CEL) gene: novel copy number variants (CNVs) identified by both classical and high-throughput genetic analysis
29. Pathogenic variants of carboxyl-ester lipase (CEL) may affect the functional properties of the normal CEL protein
30. Targeted next-generation sequencing reveals MODY in up to 6.5% of antibody-negative diabetes cases listed in the Norwegian Childhood Diabetes Registry
31. In VitroFunctional Analysis Can Aid Precision Diagnostics of Hepatocyte Nuclear Factor 1B Maturity-Onset Diabetes of the Young
32. The carboxyl-ester lipase (CEL) locus in pancreatitis: phenotypic characterization of three families carrying the CEL-HYB risk variant
33. A recombined allele of the lipase gene CEL and its pseudogene CELP confers susceptibility to chronic pancreatitis
34. Endocytosis of Secreted Carboxyl Ester Lipase in a Syndrome of Diabetes and Pancreatic Exocrine Dysfunction
35. GCK-MODY diabetes as a protein misfolding disease: The mutation R275C promotes protein misfolding, self-association and cellular degradation
36. Diabetes and pancreatic exocrine dysfunction due to mutations in the carboxyl-ester lipase gene (CEL-MODY) : a protein misfolding disease
37. SUMOylation of Pancreatic Glucokinase Regulates Its Cellular Stability and Activity*
38. Derivation of Human Induced Pluripotent Stem Cells from Patients with Maturity Onset Diabetes of the Young*
39. GCK-MODY diabetes associated with protein misfolding, cellular self-association and degradation
40. Diabetes and Pancreatic Exocrine Dysfunction Due to Mutations in the Carboxyl Ester Lipase Gene-Maturity Onset Diabetes of the Young (CEL-MODY)
41. Proteasome involvement in the degradation of the Gq family of Gα subunits.
42. Gα12 binds to the N-terminal regulatory domain of p120ctn, and downregulates p120ctn tyrosine phosphorylation induced by Src family kinases via a RhoA independent mechanism
43. Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases.
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