Ultraviolet B irradiation and activation of protein kinase D in primary mouse epidermal keratinocytes.

摘要: Our previous studies demonstrated that protein kinase D (PKD), a serine/threonine implicated in various cell processes, is upregulated basal carcinoma (BCC), supporting possible tumorigenic role for PKD skin. As the greatest risk factor BCC sun exposure, ability of ultraviolet B (UVB) irradiation to activate primary mouse keratinocytes was investigated. Using western analysis with two autophosphorylation-specific antibodies, we show first time UVB activated time- and dose-dependent manner. UVB-induced activation verified using an vitro assay. Furthermore, reduced by antioxidant pretreatment, suggesting link oxidative stress. mediated primarily Src family tyrosine kinases rather than C (PKC), fact, did not alter PKC-mediated transphosphorylation. induced apoptosis dose dependently, this death could be prevented overexpression wild-type PKD, but mutant or empty adenovirus. Indeed, cannot phosphorylated exacerbated UVB-elicited apoptosis. Thus, our data indicate induces Src-mediated which protects cells from UVB-stimulated apoptosis, providing explanation observed upregulation BCC.