jun-D: a third member of the jun gene family.

Abstract

The protooncogene c-jun encodes a component of the transcription factor AP-1. Both murine c-jun and a related gene (jun-B) are rapidly activated in BALB/c3T3 cells by serum growth factors. We report here the cloning and analysis of a cDNA encoding a third member of the murine jun family, jun-D. The amino acid sequence encoded by jun-D has two extensive regions of homology with the other Jun proteins. One homology region includes the DNA-binding domain and sequences required for dimer formation and interaction with the Fos oncoprotein; the other includes the acidic sequence thought to be involved in gene activation. All three jun mRNAs are present in a variety of murine tissues and cell lines. In resting 3T3 cells, jun-D is expressed at a higher level compared to c-jun and jun-B, and its transcription is stimulated only slightly by serum growth factors. Thus, jun-D appears to be regulated differently than c-jun and jun-B.

Effects of the inhibition of p38/RK MAP kinase on induction of five fos and jun genes by diverse stimuli

“…EGF-induced junD transcripts were detectable up to 2 h, at a similar level to that seen after 30 min stimulation. Co-treatment with SB 203580 resulted in slightly higher junD mRNA accumulation and this approximately 1.5-fold increased level was maintained over the full timecourse analysed here; this is possibly due to the intrinsic stability of these transcripts compared to that of other IE genes (Ryder et al, 1989;CAH and LCM not shown). Although elevated, the enhanced induction responses seen here were considerably lower than those observed under superinducing conditions with anisomycin (data not shown).…”

“…Note that induction of the fosB gene in response to anisomycin is generally extremely weak or undetectable. Inhibition of junD by SB 203580 is less apparent than that of c-fos, c-jun or junB; this may be due to the increased stability and persistence of these transcripts compared to that of the other IE genes studied here (Ryder et al, 1989; CAH and LCM not shown; see Figure 5). These results correlate well with the dose-dependence of inhibition of MAPKAP-K2 activation by SB 203580 in C3H 10T cells (Hazzalin et al, 1996;EC and LCM, unpublished data).…”

Identification of domains of c-Jun mediating androgen receptor transactivation

“…Wild type c-Jun and mutants cloned into either RSV-or CMV-based eukaryotic expression vectors have been previously described: c-Jun/CMV (Brown et al, 1996); c-Jun/RSV ; JunD287 ± 331 (Alani et al, 1991); the leucine zipper point mutants, M8, M9 and M14, ; internal deletion mutants, JunD194 ± 223 and JunD146 ± 221 ; JunA?D 265 In265 (Brown et al, 1996); c-Jun/v-Jun chimeras (Oehler et al, 1993); and cJun Ala63/73 (Smeal et al, 1991). JunB (Schutte et al, 1989) and JunD (Ryder et al, 1989) have been previously described. JunD1 ± 245 was constructed by using the polymerase chain reaction (PCR) to amplify c-Jun amino acids 246 ± 331.…”

Transformation by ras modifies AP1 composition and activity

“…The jun and fos families of genes are composed of three jun members (c-jun, junB, and junD) (Bohmann et al, 1987;Hirai et al, 1989;Maki et al, 1987;Ryder et al, , 1989 and four di erent fos partners (c-fos, fosB, fra1 and fra2) (Cohen and Curran, 1988;Nishina et al, 1990;Zerial et al, 1989). These genes encode components of the AP1 transcription factor formed by homo-or hetero-dimerization of the Jun and Fos proteins.…”