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. 2024 Oct 19;300(12):107907. doi: 10.1016/j.jbc.2024.107907

Figure 1.

Figure 1

Mechanisms of the heat shock response and its implications in cancer.A, damaged or misfolded proteins are triaged by HSP70 or HSP90, with or without co-chaperones HSP40 or HSP27. The preference for CHIP versus HOP determines the fate of substrates, leading to either degradation or refolding. B, a stressor promotes the interaction of CHIP with HSF1 to initiate the HSR, leading to HSF1’s translocation to the nucleus. HSF1 then activates the transcription of HSR components. Posttranslational modifications (PTMs) on HSR components can influence protein–protein interactions, localization, degradation, and transcription. These PTMs can also affect cancer proliferation and chemoresistance.