Figure 1423

Dynamics of heat shock proteins (HSP) in stressed cells. Mechanisms of activation and feedback control of the inducible heat shock gene. In the normal unstressed cell, heat shock factor (HSF) is rendered inactive by association with the con-stitutively expressed HSP70. After hypoxia or ATP depletion, partially denatured proteins (DP) become preferentially associated with HSC73, releasing HSF and allowing trimerization and binding to the heat shock element (HSE) to initiate the transcription of the heat shock gene. After translation, excess inducible HSP (HSP72) interacts with the trimer-ized HSF to convert it back to its monomeric state and release it from the HSE, thus turning off the response. (Adapted from Kashgarian [21]; with permission.)

Free Radical Pathways in the Mitochondrion Catalase/GPx complex? Hydrogen V1

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Wh^f) V^Tissue EC-SOD

fcAx

Wh^f) V^Tissue EC-SOD

Hydrogen /

peroxide

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