Insulin and insulin-like growth factor-1 stimulate dephosphorylation of paxillin in parallel with focal adhesion kinase

被引:24
|
作者
Konstantopoulos, N [1 ]
Clark, S [1 ]
机构
[1] UNIV MELBOURNE,DEPT MED,PARKVILLE,VIC 3050,AUSTRALIA
关键词
D O I
10.1042/bj3140387
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Paxillin and focal adhesion kinase (pp125(FAK)) co-localize in focal adhesions; recently insulin has been shown to stimulate the dephosphorylation of pp 125(FAK), however, its effect on paxillin is unknown. We show that insulin and IGF-1 can stimulate the dephosphorylation of paxillin in CHOT (overexpress human insulin receptors) and CHO Delta CT69 (overexpress insulin receptors lacking C-terminal 69 amino acids) cells. Furthermore, the insulin-receptor C-terminus is not needed for either insulin or IGF-1 to stimulate paxillin or pp125(FAK) dephosphorylation in the CHO (Chinese-hamster ovary) cell lines used.
引用
收藏
页码:387 / 390
页数:4
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