Heat shock factor 1 is involved in estrogen-induced chromatin remodeling in estrogen receptor-positive breast cancer cells.

A pathway controlling non-apoptotic developmental cell death engages non-canonical death-promoting activities of the stress factor HSF-1, which, in turn, activates specific components of the ubiquitin-mediated degradation machinery.

Heat-induced local unfolding allows Hsf1 to form trimers and bind to DNA, which depends on Hsf1 concentration and is promoted, not inhibited, by Hsp90.

A gene that codes for a transcription factor that is involved in lipid and carbohydrate metabolism also has a role in the regulation of circadian rhythms.

Quantitative dissection of the roles of chaperone binding and phosphorylation in regulating heat shock factor 1 leads to a predictive model of the dynamics of the yeast heat shock response.

A genome-wide screen in yeast reveals that key proteins in ribosome quality control also regulate mutant Huntingtin aggregation and toxicity.

Neuronal serotonin release tunes transcription response times of Caenorhabditis elegans germ cells to promote the survival and stress resistance of future offspring.

Dynamic regulation of the heat shock response depends on a negative feedback loop in which Hsf1 activates expression of Hsp70 and Hsp70 specifically and directly represses Hsf1 transactivation.

Hsp70 restricts DNA binding activity of Hsf1 to control the width and amplitude of the heat-shock regulon.

Endo-siRNAs slow down the rate of aging and enable the maintenance of a responsive heat shock response in aging germline-less Caenorhabditis elegans.