Exendin‐4 overcomes cytokine‐induced decreases in gap junction coupling via protein kinase A and Epac2 in mouse and human islets
Author:
Affiliation:
1. Barbara Davis Center for Childhood DiabetesUniversity of Colorado Anschutz Medical Campus Aurora CO 80045 USA
2. Department of BioengineeringUniversity of Colorado Anschutz Medical Campus Aurora CO 80045 USA
Funder
National Institutes of Health
Juvenile Diabetes Research Foundation International
Publisher
Wiley
Subject
Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1113/JP276106
Reference65 articles.
1. Exendin 4 controls insulin production in rat islet beta cells predominantly by potentiation of glucose-stimulated proinsulin biosynthesis at the translational level
2. Connexin36 contributes to INS-1E cells survival through modulation of cytokine-induced oxidative stress, ER stress and AMPK activity
3. Cytokine-Induced Inhibition of Insulin Release from Mouse Pancreatic β-Cells Deficient in Inducible Nitric Oxide Synthase
4. Biphasic increase of gap junction coupling induced by dipyridamole in the rat aortic A-10 vascular smooth muscle cell line
5. The transcriptional landscape of mouse beta cells compared to human beta cells reveals notable species differences in long non-coding RNA and protein-coding gene expression
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