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ATF2Activating Transcription Factor 2
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On the other hand, G[[alpha].sub.12/13]/RhoA/ROCK signaling causes activation of transcription factor ATF2 to induce further proinflammatory mediator production.
A synthetic 3'-UTR of ATF2 with the putative miR-204/211 seed region was inserted into the multiple cloning site of the pmiR-RB-Report (Thermo Fisher, USA) vector.
Furthermore, ROS activate the phosphorylation of the transcription factors c-Jun and ATF2, thereby increasing the expression of their target genes, including ANGPTL2 itself [27, 28].
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].
A recent study indicated that AST could have a direct effect on c-Jun-N-terminal kinase 1, which regulates numerous factors downstream of c-Jun, such as ATF2, SMAD4, and HSF1.
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.