The transcription factor ATF-2 (also called CRE-BP1) binds to both AP-1 and CRE DNA response elements and is a member of the ATF/CREB family of leucine zipper proteins (1). ATF-2 is known to interact with a variety of viral oncoproteins and cellular tumor suppressors and has been shown to be a target of the SAPK/JNK and p38 MAP kinase signaling pathways (2–4). Various forms of cellular stress including genotoxic agents, inflammatory cytokines and UV irradiation stimulate the transcriptional activity of ATF-2. Cellular stress activates ATF-2 by phosphorylation of Thr69 and Thr71 (2–4). Both SAPK and p38 MAPK have been shown to phosphorylate ATF-2 at these sites in vitro and in cells transfected with ATF-2. Mutations of these sites result in the loss of stress induced transcription by ATF-2 (2–4). In addition, mutations at these sites also reduce the ability of E1A and Rb to stimulate gene expression via ATF-2 (2).

NIH/3T3 cells

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