Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes-Reference-Cited by-同舟云学术

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Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes

Published:2007-11 Issue:s2 Volume:9 Page:46-55
ISSN:1462-8902
Container-title:Diabetes, Obesity and Metabolism
language:en
Short-container-title:Diabetes Obes Metab

Author:

Tarasov A. I.,Girard C. A.,Larkin B.,Tammaro P.,Flanagan S. E.,Ellard S.,Ashcroft F. M.

Publisher

Wiley

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism,Internal Medicine

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1463-1326.2007.00777.x/fullpdf

Reference35 articles.

1. Type 2 diabetes mellitus: not quite exciting enough?

2. ATP-sensitive potassium channelopathies: focus on insulin secretion

3. Activating Mutations in Kir6.2 and Neonatal Diabetes

4. Association and Stoichiometry of KATP Channel Subunits

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1. Integrative Study of the Structural and Dynamical Properties of a KirBac3.1 Mutant: Functional Implication of a Highly Conserved Tryptophan in the Transmembrane Domain;International Journal of Molecular Sciences;2021-12-29

2. Imaging Meets Cytometry: Analyzing Heterogeneous Functional Microscopic Data from Living Cell Populations;Journal of Imaging;2021-01-13

3. New insights into KATP channel gene mutations and neonatal diabetes mellitus;Nature Reviews Endocrinology;2020-05-06

4. Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk;Diabetologia;2016-04-27

5. ATP-Sensitive Potassium Channels in Health and Disease;Islets of Langerhans;2014-05-30

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