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cAMP promotes pancreatic β-cell survival via CREB-mediated induction of IRS2
Open accessAbstract
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 β-cells, develop diabetes secondary to β-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 IRS2by 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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Metadata
- Authors
- Jhala, U. S., Canettieri, G., Screaton, R. A., Kulkarni, R. N., Krajewski, S., Reed, J., Walker, J., Lin, X., White, M., & Montminy, M.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2003-07-01
- Volume
- 17
- Issue
- 13
- Pages
- 1575-1580
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2165991181
- Cited by
- 543
- References
- 1
- Type
- posted content
- Language
- en
- Open access
- diamond
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