Hyperinsulinemic hypoglycemia subtype glucokinase V91L mutant induces necrosis in β-cells via ATP depletion-Reference-Cited by-同舟云学术

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Hyperinsulinemic hypoglycemia subtype glucokinase V91L mutant induces necrosis in β-cells via ATP depletion

Published:2019-03 Issue: Volume:17 Page:108-113
ISSN:2405-5808
Container-title:Biochemistry and Biophysics Reports
language:en
Short-container-title:Biochemistry and Biophysics Reports

Author:

Lu Brian,Tonne Jason M.,Munoz-Gomez Miguel,Ikeda Yasuhiro

Funder

Vann Family Fund in Diabetes Research

Kieckhefers Foundation

Paul A. and Ruth M. Schilling Medical Research Endowment Fund

Mayo Clinic Center for Regenerative Medicine

Mayo Clinic Graduate School of Biomedical Sciences

Initiative for Maximizing Student Development

Publisher

Elsevier BV

Subject

Biochemistry,Biophysics

Reference31 articles.

1. Glucose regulates cyclin D2 expression in quiescent and replicating pancreatic β-cells through glycolysis and calcium channels;Salpeter;Endocrinology,2011

2. Control of pancreatic β cell regeneration by glucose metabolism;Porat;Cell Metab.,2011

3. Update on mutations in glucokinase (GCK), which cause maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemic hypoglycemia;Osbak;Hum. Mutat.,2009

4. Cross-sectional and longitudinal studies suggest pharmacological treatment used in patients with glucokinase mutations does not alter glycaemia;Stride;Diabetologia,2014

5. Recognition and management of individuals with hyperglycemia because of a heterozygous glucokinase mutation;Chakera;Diabetes Care,2015

Cited by 1 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. The novel GCK variant p.Val455Leu associated with hyperinsulinism is susceptible to allosteric activation and is conducive to weight gain and the development of diabetes;Diabetologia;2021-09-16

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