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

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作者： Raimondo, Anne ^[1] ; Chakera, Ali J. ^[2] ; Thomsen, Soren K. ^[3] ; Colclough, Kevin ^[4] ; Barrett, Amy ^[5] ; De Franco, Elisa ^[6] ; Chatelas, Alisson ; Demirbilek, Huseyin ; Akcay, Teoman ; Alawneh, Hussein ; Flanagan, Sarah E. ; Van De Bunt, Martijn ; Hattersley, Andrew T. ; Gloyn, Anna L. ; Ellard, Sian

作者单位： Royal Devon & Exeter NHS Fdn Trust, Mol Genet Lab, Exeter EX2 5DW, Devon, England ^[1] Queen Rania Al Abdullah Hosp Children, King Hussein Med Ctr, Royal Med Serv, Pediat Endocrine Div ^[2] Churchill Hosp, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX3 7LE, England ^[3] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Exeter EX2 5DW, Devon, England ^[4] Dr Sadi Konuk Educ & Res Hosp, Div Pediat Endocrinol, TR-34147 Istanbul, Turkey ^[5] Diyarbakir Children State Hosp, Dept Paediat Endocrinol, TR-21100 Diyarbakir, Turkey ^[6]

发布时间 2015-05-03

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Human Molecular Genetics

2014年23卷24期

6432-6440页

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

Human Molecular Genetics

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Human Molecular Genetics

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

Human Molecular Genetics

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Human Molecular Genetics

相关期刊

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