Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 285, Issue 4, Pages E669-E684Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00196.2003
Keywords
cytokines; posttranslational modifications; histidine phosphorylation; diabetes mellitus; pancreatic islet
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Funding
- NIDDK NIH HHS [DK-56005] Funding Source: Medline
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Emerging evidence suggests that GTP-binding proteins ( G proteins) play important regulatory roles in physiological insulin secretion from the islet beta-cell. Such conclusions were drawn primarily from experimental data derived through the use of specific inhibitors of G protein function. Data from gene depletion experiments appear to further substantiate key roles for these signaling proteins in the islet metabolism. The first part of this review will focus on findings supporting the hypothesis that activation of specific G proteins is essential for insulin secretion, including regulation of their function by posttranslational modifications at their COOH-terminal cysteines ( e. g., isoprenylation). The second part will overview novel, non-receptor-dependent mechanism(s) whereby glucose might activate specific G proteins via protein histidine phosphorylation. The third section will review findings that appear to link abnormalities in the expression and/or functional activation of these key signaling proteins to impaired insulin secretion. It is hoped that this review will establish a basis for future research in this area of islet signal transduction, which presents a significant potential, not only in identifying key signaling proteins that are involved in physiological insulin secretion, but also in examining potential abnormalities in this signaling cascade that lead to islet dysfunction and onset of diabetes.
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