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Diagram illustrating key interactions among E2, NFκB, HSF-1, and heat shock proteins (HSPs). Acute E2 treatment leads to NFκB activation and induction of genes responsible for cell survival and inflammation. NFκB activates HSF-1, which then induces HSPs. HSF-1 activation can suppress expression of inflammatory cytokines, such as TNF-α directly, or indirectly inhibit apoptosis and NFκB activation through HSP expression.
