HSF1


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HSF1

A gene on chromosome 8q24.3 that encodes a member of the DNA-binding heat-shock transcription factor family, which are rapidly induced by temperature and other forms of intracellular stress. HSF1 is repressed by Hsp90 and/or multi-chaperone complexes.
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Heat stress (H + W) induced a slight increase in the expression level of both HSF3 and HSF1. This effect was significantly increased when blue light was applied during heat stress (H + B).
HSP90 is one of the heat shock proteins reported to function as multichaperone complexes by combining with different cochaperones (Cdc37, p23, Hop, pP5, SGT1, Aha 1, etc.) affecting binding ability of HSP90 to client proteins (AKT, KIT, ErbB2, CDK 4, HSF1, Apaf-1, MMp2, etc.) [43].
Overexpression of HSP-70 inhibits the phosphorylation of HSF1 by activating protein phosphatase and inhibiting protein kinase C activity.
The HSF1 "plays a crucial role in the response of brain cells to prenatal environmental insults," the researchers reported.
Both Hsps regulate the activation of the HSF1 transcription factor, which is linked to the transcriptional stress response [33, 34].
Induction of heat shock proteins by hyperthermia and noise overstimulation in hsf1 -/- mice.
Estas ultimas se encuentran sobre la superficie celular siendo regulada su expresion por el factor de transcripcion Hsf1; se les atribuye un papel en el cambio de forma de levadura a hifa (25).
The member of the Hsf family, Hsf1 is involved in the Hsps induction owed to heat shock and other kinds of stress (8-10).
The gene, called heat-shock factor 1 (Hsf1), doesn't itself trigger cancer.
In addition, decreases in ATP levels have been previously found to elicit the induction of HSPs by DNA binding and activation of the transcriptional factor HSF1 (39).
In NAFLD&NASH, we observed that oxidative stress could activate epidermal growth factor receptor (EGFR) to facilitate (i) UBC to repress HSF1 in the WNT and MAPK signaling pathways; (ii) APP to activate ETS1 in the MAPK signaling pathway to induce DNA repair function through the mediation of RFC5, to activate metabolism through the mediation of TRMT1, and to inhibit apoptosis through the mediation of ZNF480; and (iii) SHC1 to repress STAT5A in the MAPK signaling pathway.
We lack an overarching view of how, Despite being genomically stable, The tme is heterogeneously reprogrammed across time and space to promote evolution of aggressive disease.recently i discovered that heat-shock factor 1 (hsf1), A cytoprotective transcription factor (tf), Is vital to this reprogramming, Promoting malignancy in patients and mice upon activation in the stroma.