A wound-induced keratin inhibits Src activity during keratinocyte migration and tissue repair.

ABSTRACT: Injury to the epidermis triggers an elaborate homeostatic response resulting in tissue repair and recovery of the vital barrier function. The type II keratins 6a and 6b (K6a and K6b) are among the genes induced early on in wound-proximal keratinocytes and maintained during reepithelialization. Paradoxically, genetic ablation of K6a and K6b results in enhanced keratinocyte migration. In this paper, we show that this trait results from activation of Src kinase and key Src substrates that promote cell migration. Endogenous Src physically associated with keratin proteins in keratinocytes in a K6-dependent fashion. Purified Src bound K6-containing filaments via its SH2 domain in a novel phosphorylation-independent manner, resulting in kinase inhibition. K6 protein was enriched in the detergent-

SUBMITTER: Rotty JD 

PROVIDER: S-EPMC3341159 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature