- E-mailBente.Johansson@uib.no
- Phone+47 924 61 675+47 55971263
- Visitor AddressHaukeland universitetssykehus, Laboratoriebygget5009 Bergen
- Postal AddressPostboks 78045020 Bergen
Academic article
- (2022). Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases. Journal of Clinical Endocrinology and Metabolism (JCEM). e1455-e1466.
- (2022). Characterization of the genetic architecture of infant and early childhood body mass index. Nature Metabolism. 344-358.
- (2022). Abnormal exocrine–endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8. Nature Metabolism. 76-89.
- (2021). The position of single-base deletions in the VNTR sequence of the carboxyl ester lipase (CEL) gene determines proteotoxicity. Journal of Biological Chemistry. 1-13.
- (2021). Protein misfolding in combination with other risk factors in CEL-HYB1-mediated chronic pancreatitis. European Journal of Gastroenterology and Hepathology. 839-843.
- (2020). Pathogenic Carboxyl Ester Lipase (CEL) Variants Interact with the Normal CEL Protein in Pancreatic Cells . Cells. 1-19.
- (2020). Characterization of CEL-DUP2: Complete duplication of the carboxyl ester lipase gene is unlikely to influence risk of chronic pancreatitis. Pancreatology (Print). 377-384.
- (2018). 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. Journal of Biological Chemistry. 19476-19491.
- (2017). Targeted next-generation sequencing reveals MODY in up to 6.5% of antibody-negative diabetes cases listed in the Norwegian Childhood Diabetes Registry. Diabetologia. 625-635.
- (2017). Nuclear import of glucokinase in pancreatic beta-cells is mediated by a nuclear localization signal and modulated by SUMOylation. Molecular and Cellular Endocrinology. 146-157.
- (2017). Copy number variants and VNTR length polymorphisms of the carboxyl-ester lipase (CEL) gene as risk factors in pancreatic cancer. Pancreatology (Print). 83-88.
- (2015). Glycogenin-2 is dispensable for liver glycogen synthesis and glucagon-stimulated glucose release. Journal of Clinical Endocrinology and Metabolism (JCEM). E767-E775.
- (2015). A recombined allele of the lipase gene CEL and its pseudogene CELP confers susceptibility to chronic pancreatitis. Nature Genetics. 518-522.
- (2014). GCK-MODY diabetes as a protein misfolding disease: The mutation R275C promotes protein misfolding, self-association and cellular degradation. Molecular and Cellular Endocrinology. 55-65.
- (2014). Endocytosis of secreted carboxyl ester lipase in a syndrome of diabetes and pancreatic exocrine dysfunction. Journal of Biological Chemistry. 29097-29111.
- (2013). SUMOylation of pancreatic glucokinase regulates its cellular stability and activity. Journal of Biological Chemistry. 5951-5962.
- (2013). SHORT syndrome with partial lipodystrophy due to impaired phosphatidylinositol 3 kinase signaling. American Journal of Human Genetics. 150-157.
- (2013). Prevalence of monogenic diabetes in the population-based Norwegian Childhood Diabetes Registry. Diabetologia. 1512-1519.
- (2013). Derivation of Human Induced Pluripotent Stem Cells from Patients with Maturity Onset Diabetes of the Young. Journal of Biological Chemistry. 5353-5356.
- (2012). GCK-MODY diabetes associated with protein misfolding, cellular self-association and degradation. Biochimica et Biophysica Acta - Molecular Basis of Disease. 1705-1715.
- (2011). Gα(12) binds to the N-terminal regulatory domain of p120(ctn), and downregulates p120(ctn) tyrosine phosphorylation induced by Src family kinases via a RhoA independent mechanism. Experimental Cell Research. 293-306.
- (2011). G alpha(12) binds to the N-terminal regulatory domain of p120(ctn), and downregulates p120(ctn) tyrosine phosphorylation induced by Src family kinases via a RhoA independent mechanism. Experimental Cell Research. 293-306.
- (2011). Diabetes and pancreatic exocrine dysfunction due to mutations in the carboxyl ester lipase gene-maturity onset diabetes of the young (CEL-MODY) A PROTEIN MISFOLDING DISEASE. Journal of Biological Chemistry. 34593-34605.
- (2005). Proteasome involvement in the degradation of the G(q) family of G alpha subunits. The FEBS Journal. 5365-5377.
Academic lecture
- (2002). Proteasome involvement in the degradation of Galpha 16 and Galpha q.
Doctoral dissertation
- (2006). Interacting partners of the Gαq and Gα12 subunits of the heterotrimeric G proteins.
Abstract
- (2013). Cellular re-uptake of secreted carboxyl-ester lipase protein in CEL-MODY, a syndrome of diabetes and pancreatic exocrine dysfunction. Diabetologia. S152-S152.
- (2008). Pancreatic exocrine dysfunction in diabetes: functional characterisation of the carboxyl-ester lipase gene. Diabetologia. S123-S124.
Poster
- (2018). Functional characterization of HNF1A variants identified in Norwegian diabetes registries can be important for precision medicine in diabetes clinics.
- (2002). Mechanism of regulation of Galpha 16 and Galpha q.
- (2001). Mechanisms og regulation and degradation of Galpha16 and Galphaq.
- (2001). Mechanisms of regulation and degradation of Galpha16 and GalphaQ.
Academic literature review
- (2018). The role of the carboxyl ester lipase (CEL) gene in pancreatic disease. Pancreatology (Print). 12-19.
More information in national current research information system (CRIStin)