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

Paxillin and focal adhesion kinase (pp125FAK) co-localize in focal adhesions; recently insulin has been shown to stimulate the dephosphorylation of pp125FAK; 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 pp125FAK dephosphorylation in the CHO (Chinese-hamster ovary) cell lines used.