Journal
GENES & DEVELOPMENT
Volume 17, Issue 13, Pages 1575-1580Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1097103
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Funding
- NIDDK NIH HHS [DK49777, DK43828, R01 DK049777] Funding Source: Medline
- NIGMS NIH HHS [R37 GM037828, GM37828] Funding Source: Medline
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The incretin hormone GLP1 promotes islet-cell survival via the second messenger cAMP. Here we show that mice deficient in the activity of CREB, caused by expression of a dominant-negative A-CREB transgene in pancreatic beta-cells, develop diabetes secondary to beta-cell apoptosis. Remarkably, A-CREB severely disrupted expression of IRS2, an insulin signaling pathway component that is shown here to be a direct target for CREB action in vivo. As induction of IRS2 by cAMP enhanced activation of the survival kinase Akt in response to insulin and IGF-1, our results demonstrate a novel mechanism by which opposing pathways cooperate in promoting cell survival.
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