期刊
JOURNAL OF GENERAL PHYSIOLOGY
卷 132, 期 3, 页码 329-338出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1085/jgp.200810044
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资金
- Ellison Medical Foundation
- American Diabetes Association
- Hirschl-Weil Cauler Trust
- National Institutes of Health [GM62328, DA007274]
- Tri-Institutional MSTP
- Barbara and Stephen Friedman Fellowship
In beta cells, both glucose and hormones, such as GLP-1, stimulate production of the second messenger cAMP, but glucose and GLP-1 elicit distinct cellular responses. We now show in INS-1E insulinoma cells that glucose and GLP-1 produce cAMP with distinct kinetics via different adenylyl cyclases. GLP-1 induces a rapid cAMP signal mediated by G protein-responsive transmembrane adenylyl cyclases (tmAC). In contrast, glucose elicits a delayed cAMP rise mediated by bicarbonate, calcium, and ATP-sensitive soluble adenylyl cyclase (sAC). This glucose-induced, sAC-dependent cAMP rise is dependent upon calcium influx and is responsible for the glucose-induced activation of the mitogen-activated protein kinase (ERK1/2) pathway. These results demonstrate that sAC-generated and tmAC-generated cAMP define distinct signaling cascades.
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