Transactivation of Fra-1 and consequent activation of AP-1 occur extracellular signal-regulated kinase dependently.

ABSTRACT: Mitogen-activated protein (MAP) kinase, extracellular-signal-regulated kinases (ERKs) play an important role in activating AP-1-dependent transcription. Studies using the JB6 mouse epidermal model and a transgenic mouse model have established a requirement for AP-1-dependent transcription in tumor promotion. Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor induce activator protein 1 (AP-1) activity and neoplastic transformation in JB6 transformation-sensitive (P(+)) cells, but not in transformation-resistant (P(-)) variants. The resistance in one of the P(-) variants can be attributed to the low levels of the MAP kinases, ERKs 1 and 2, and consequent nonresponsiveness to AP-1 activation. The resistant variant is not deficient in c-fos transcrip

SUBMITTER: Young MR 

PROVIDER: S-EPMC139745 | biostudies-literature | 2002 Jan

REPOSITORIES: biostudies-literature