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Hsf1 ck2

Teruya Tamaru, Masaaki Ikeda
The circadian clock system confers daily anticipatory physiological processes with the ability to be reset by environmental cues. This "circadian adaptation system" (CAS), driven by cell-autonomous molecular clocks, orchestrates various rhythmic physiological processes in the entire body. Hence, the dysfunction of these clocks exacerbates various diseases, which may partially be due to the impairment of protective pathways. If this is the case, how does the CAS respond to cell injury stresses that are critical in maintaining health and life by evoking protective pathways? To address this question, here we review and discuss recent evidence revealing life-protective (pro-survival) molecular networks between clock (e...
July 2016: Journal of Physiological Sciences: JPS
Bo-Ram Cho, Peter Lee, Ji-Sook Hahn
Ethanol, the major fermentation product of Saccharomyces cerevisiae, has long been known as an inducer of heat shock response, but the underlying mechanisms by which ethanol activates heat shock transcription factor (HSF) are not well understood. We demonstrate that CK2-dependent phosphorylation on S608 is an ethanol stress-specific repression mechanism of Hsf1, which does not affect the basal or heat-induced activity of Hsf1. This repression is relieved by dephosphorylation by Ppt1 which directly interacts with Hsf1 via its tetratricopeptide repeat (TPR) domain...
July 2014: Molecular Microbiology
Teruya Tamaru, Mitsuru Hattori, Yasuharu Ninomiya, Genki Kawamura, Guillaume Varès, Kousuke Honda, Durga Prasad Mishra, Bing Wang, Ivor Benjamin, Paolo Sassone-Corsi, Takeaki Ozawa, Ken Takamatsu
Dysfunction of circadian clocks exacerbates various diseases, in part likely due to impaired stress resistance. It is unclear how circadian clock system responds toward critical stresses, to evoke life-protective adaptation. We identified a reactive oxygen species (ROS), H2O2 -responsive circadian pathway in mammals. Near-lethal doses of ROS-induced critical oxidative stress (cOS) at the branch point of life and death resets circadian clocks, synergistically evoking protective responses for cell survival. The cOS-triggered clock resetting and pro-survival responses are mediated by transcription factor, central clock-regulatory BMAL1 and heat shock stress-responsive (HSR) HSF1...
2013: PloS One
Fabrice Soncin, Xinfeng Zhang, Boyang Chu, Xiaozhe Wang, Alexzander Asea, Mary Ann Stevenson, David B Sacks, Stuart K Calderwood
Heat shock factor-1 (HSF-1) is the regulator of hsp molecular chaperone transcription, although the intracellular mechanisms involved in HSF-1 activation have not been fully elucidated. As HSF1 is activated by heat shock simultaneously with the nuclear translocation of the protein kinase CK2, we have investigated the role of CK2 in HSF1 activation. We demonstrate that HSF-1 is phosphorylated by CK2 on both serine and threonine residues and has characterized a phosphorylation site at threonine 142. Mutation of Thr-142 to alanine (T142A) inhibits trans-activation of the HSP70 gene by HSF1 and in addition inhibits the accumulation of HSF-1 competent to bind heat shock elements in the nucleus...
April 4, 2003: Biochemical and Biophysical Research Communications
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