Phosphorylation and high level expression of Fra-2 in v-src transformed cells: a pathway of activation of endogenous AP-1

Overexpression of fra-2 in transgenic mice perturbs normal eye development

“…Interestingly, several oncogenes, namely v-yes, v-fps, c-Ha-ras and activated c-raf, cause an elevation in fra-2 expression . The Fra-2 protein is a substrate for phosphorylation by the MAP kinase ERK2, and in v-src transformed cells there is an increase in both ERK2 activity and in the phosphorylation of the Fra-2 protein (Murakami et al, 1997). It has been suggested that phosphorylation of Fra-2 may convert it from an ine cient transcriptional activator into an active one.…”

Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis

“…Experimental overexpression of cJun and/or Fra1 in immortalized rodent ®broblasts is su cient to induce oncogenic transformation in the absence of Ras (Mechta et al, 1997;Bergers et al, 1995). In chicken embryo ®broblasts transformation by v-Src and active versions of Ras and Raf is accompanied by enhanced levels of c-Jun and Fra2, and, in addition, Fra2 hyperphosphorylation (Muramaki et al, 1997;Suzuki et al, 1994).…”

Kinetics of v-src-induced epithelial–mesenchymal transition in developing glandular stomach

“…We monitored GFP fluorescence in the organ culture on day 2 and found that all the vectors except for MEKDD caused no apparent morphological effects. We have previously shown that exogenous expression of MEKDD in CEF caused activation of endogenous MAP kinase (ERK2), although the level of the active form of ERK2 in these cells was lower than that in v-srcexpressing cells (Murakami et al, 1997a(Murakami et al, , 1999, and our …”

“…One function of v-src, for example, isolated from Rous sarcoma virus (RSV), is to elevate endogenous MAP kinase activity constitutively in chicken embryo fibroblasts (CEF), which, in turn, leads to activation of transcription factor AP-1 (c-jun and fra-2) through autoregulatory loops (Suzuki et al, 1994;Murakami et al, 1997aMurakami et al, , 1999. Another transcription factor, Stat 3, was also shown to be activated in fibroblasts (Zhang et al, 2000), possibly through a different signaling pathway that involves Jak1 kinase.…”