ATF1, CREB, and CREM constitute a subfamily of the basic leucine zipper transcription factors, and they activate gene expression by binding as homo- or heterodimers to the cAMP response elements (CRE) (consensus: 5'-GTGACGT[AC][AG]-3'). ATF1 (activating transcription factor 1) plays important roles in cell survival and proliferation [, ]. It is required for the development of preimplantation embryos [].
This entry represents ribosomal protein S6 kinase II []. This enzyme acts as a serine/threonine kinase required for the mitogen or stress-induced phosphorylation of the transcription factors CREB (cAMP response element-binding protein) and ATF1 (activating transcription factor-1). It plays an essential role in the control of RELA transcriptional activity in response to TNF. It directly represses transcription via phosphorylation of Ser-1 of histone H2A. It phosphorylates Ser-10 of histone H3 in response to mitogenics, stress stimuli and epidemal growth-factor (EGF), which results in the transcriptional activation of several immediate early genes, including proto-oncogenes c-fos/FOS and c-jun/JUN. It mediates the mitogen- and stress-induced phosphorylation of high mobility group protein 14 (HMG-14). It requires magnesium ions as a cofactor.
This family is composed of the mitogen-activated protein kinases (MAPKs) Sty1 from Schizosaccharomyces pombe, Hog1 from Saccharomyces cerevisiae, and similar fungal proteins. Sty1 and Hog1 are stress-activated MAPKs that participate in transcriptional regulation in response to stress [].Sty1 is activated in response to oxidative stress, osmotic stress, and UV radiation [, ]. It is regulated by the MAP2K Wis1, which is activated by the MAP3Ks Wis4 and Win1, which receive signals of the stress condition from membrane-spanning histidine kinases Mak1-3 []. Activated Sty1 stabilizes the Atf1 transcription factor and induces transcription of Atf1-dependent genes of the core environmental stress response [, ].Hog1 is the key element in the high osmolarity glycerol (HOG) pathway and is activated upon hyperosmotic stress. Activated Hog1 accumulates in the nucleus and regulates stress-induced transcription []. The HOG pathway is mediated by two transmembrane osmosensors, Sln1 and Sho1 [].
