Complexes of p21RAS with JUN N-terminal kinase and JUN proteins.

摘要: Abstract RAS gene-encoded p21 protein has been found to increase in vitro phosphorylation of JUN via its kinase, N-terminal kinase (JNK). This effect is mediated by increased JNK the presence wild-type and oncogenic (Val-12) a dose-dependent manner. Oncogenic more potent mediating this than normal counterpart. Both proteins bind purified that present cell extracts from transformed fibroblasts melanoma cells. have also bacterially expressed protein. binding dose dependent, enhanced GTP, depends on first 89 amino acids (the delta domain), as it does not occur with v-jun. While ability both strongly inhibited peptide corresponding aa 96-110, weakly 115-126, p21-JUN interaction peptides 96-110 and, lesser degree, 35-47. The results suggest interacts specifically proteins.