Fig. 8: A scheme showing RIP140 modulating HSR (by co-repressing HSF1) under different stress conditions

a In unstressed cells, HSF1, localized in the cytosol, is unable to activate its target genes. b During mild stress, HSF1 translocates to the nucleus to bind HSE and activate its chromatin targets; but RIP140 associates with HSF1 to suppress/dampen HSF1’s transcriptional activity. c In stressed cells, Syk is activated to phosphorylate RIP140 for its degradation; the suppression of HSF1 is thus relieved, enabling a full scale HSR that facilitates adaptation and recovery