Mca. Duyndam et al., The N-terminal transactivation domain of ATF2 is a target for the co-operative activation of the c-jun promoter by p300 and 12S E1A, ONCOGENE, 18(14), 1999, pp. 2311-2321
The adenovirus EIA proteins activate the c-jun promoter through two Jun/ATF
-binding sites, jun1 and jun2. P300, a transcriptional coactivator of sever
al AP1 and ATF transcription factors has been postulated to play a role in
this activation, Here,,ve present evidence that p300 can control c-jun tran
scription by acting as a cofactor for ATF2: (1) Over-expression of p300 mas
found to stimulate c-jun transcription both in the presence and absence of
EIA. (2) Like E1A, p300 activates the c-jun promoter through the jun1 and
jun2 elements and preferentially activates the N-terminal domain of ATF2. (
3) Co-immunoprecipitation assays of crude cell extracts indicate that endog
enous p300/CBP(-like) proteins and ATF2 proteins are present in a multiprot
ein complex that can bind specifically to the jun2 element, We further demo
nstrate that the Stress-Activated-Protein-Kinase (SAPK) target sites of ATF
2, Thr69 and Thr71 are not required for the formation of the p300/CBP-ATF2
multiprotein complex. These data indicate that E1A does not inhibit all tra
nscription activation functions of p300, and, in fact, cooperates with p300
in the activation of the ATF2 N-terminus.