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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.

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

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

Interplay between FGF-induced bHLH transcription factors and BMP-induced bHLH inhibitory id genes govern mesodermal cell fate choice along the mediolateral axis in both zebrafish and mouse.

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.

Carefully controlling the level of protein synthesis reduction and mode of translation inhibitor action reveal different and sometimes opposing phenotypic effects following proteostasis stress, wherein protection via initiation inhibition specifically depends on heat shock factor 1.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

The maintenance of diverse cell identities might be coordinated through the interaction between widely acting transcriptional corepressors and cell-specific transcription factors to repress undesired gene expression in a cell-type-specific manner.

Specific to muscles and essential for their development, desmin is revealed to be fundamental to the mechanics and shape maintenance of model muscle tissue even in early differentiating and unorganized systems through an integrated magnetic tensiometer approach.