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Protein prenylation in glucose-induced insulin secretion from the pancreatic islet β cell:: a perspective
被引:28
作者:
Kowluru, Anjaneyulu
[1
,2
]
机构:
[1] Wayne State Univ, Dept Pharmaceut Sci, Eugene Applebaum Coll Pharm & Hlth Sci, Detroit, MI 48201 USA
[2] John D Dingell VA Med Ctr, Beta Cell Biochem Res Lab, Detroit, MI USA
关键词:
insulin secretion;
islet beta cell;
G-proteins;
protein prenylation;
protein farnesylation;
protein geranylgeranylation;
Rac1;
Cdc42;
D O I:
10.1111/j.1582-4934.2007.00168.x
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Insulin secretion from the pancreatic beta cell is regulated principally by the ambient concentration of glucose. However, the molecular and cellular mechanisms underlying the stimulus - secretion coupling of glucose-stimulated insulin secretion (GSIS) remain only partially understood. Emerging evidence from multiple laboratories suggests key regulatory roles for GTP-binding proteins in the cascade of events leading to GSIS. This class of signalling proteins undergoes a series of requisite post-translational modifications (e.g. prenylation) at their C-terminal cysteines, which appear to be necessary for their targeting to respective membranous sites for optimal interaction with their respective effector proteins. This communication represents a perspective on potential regulatory roles for protein prenylation steps (i.e. protein farnesylation and protein geranylgeranylation) in GSIS from the islet beta cell.Possible consequences of protein prenylation and potential mechanisms underlying glucose-induced regulation of prenylation, specifically in the context of GSIS, are also discussed.
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页码:164 / 173
页数:10
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