Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion-Reference-Cited by-同舟云学术

Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion

Published:2016-10-18 Issue:12 Volume:157 Page:4534-4541
ISSN:0013-7227
Container-title:Endocrinology
language:en
Short-container-title:

Author:

Syring Kristen E.¹,Boortz Kayla A.¹,Oeser James K.¹,Ustione Alessandro²,Platt Kenneth A.³,Shadoan Melanie K.³,McGuinness Owen P.¹,Piston David W.¹,Powell David R.³,O’Brien Richard M.¹

Affiliation:

1. Department of Molecular Physiology and Biophysics (K.E.S., K.A.B., J.K.O., O.P.M., R.M.O.), Vanderbilt University Medical School, Nashville, Tennessee 37232;

2. Department of Cell Biology and Physiology (A.U., D.W.P.), Washington University School of Medicine, St. Louis, Missouri 63110;

3. Lexicon Pharmaceuticals Incorporated (K.A.P., M.K.S., D.R.P.), The Woodlands, Texas 77381

Publisher

The Endocrine Society

Subject

Endocrinology

Link

http://academic.oup.com/endo/article-pdf/157/12/4534/10841566/endo4534.pdf

Reference25 articles.

1. Zinc transporter 8 (ZnT8) and β cell function;Davidson;Trends Endocrinol Metab,2014

2. SLC30A8 mutations in type 2 diabetes;Rutter;Diabetologia,2015

3. Polymorphisms in the TCF7L2, CDKAL1 and SLC30A8 genes are associated with impaired proinsulin conversion;Kirchhoff;Diabetologia,2008