ATF2 was also shown to regulate expression of CFIOP (Averous et al.
It is also clear that some AP1 transcription factors function as procancer proteins (e.g., c-jun, c-fos), while others inhibit cancer development (e.g., JunB,
ATF2).
The study, demonstrates that the MITF is subject to negative regulation by
ATF2, and such regulation is a key determinant in melanoma development.
AtfA and its orthologues (e.g., Atf1 in the fission yeast Schizosaccharomyces pombe or
Atf2 in mammals) are conserved bZIP oxidative stress response elements regulated by MAPK (mitogen-activated protein kinase) pathways in eukaryotes [12, 13].
The general consensus is that cold stimulates a greater release of catecholamines by the nervous system, an event that stimulates thermogenesis through the activation of protein kinase A (PKA) and p38 mitogen-activated protein kinases (p-38 MAPK) pathways followed by the activation of uncoupling protein 1 (UCP1) and phosphorylation of the specific factors PPAR gamma coactivator 1 alpha (PGC-1[alpha]), cAMP response element-binding protein (cReB), and activating transcription factor 2 (
ATF2) [14,15, 44, 45].
In this study, the authors demonstrate the involvement of Gi/o, ERK, p38, and the transcription factor
ATF2 in this SCFA-induced expression [28].
Nrfl in a complex with fosB, c-jun, junD and
ATF2 forms the AP1 componet at the TNF-[alpha] promoter in stimulated mast cells, Nucleic Acid Res.
Moreover, torilin arrested AP1 transactivation and its subunits (
ATF2, c-jun, and c-fos) phosphorylation.