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SHs are synthesized from cholesterol in the adrenal cortex (glucocorticoids, mineralocorticoids, and adrenal androgens), the testes (testicular androgens, estrogen), and the ovary and placenta (estrogen and progestogen or progestins) (Payne AH & Hales DB 2004; Hu J et al. 2010;). SHs reach their target cells via the blood, where they are bound to specific carrier proteins (Grishkovskaya I et al. 2000; Hammond GL 2016). SHs detach from the carrier proteins and because of their lipophilic nature readily diffuse through the plasma membrane of cells (Oren I et al. 2004). Within the target cells SHs bind to steroid hormone receptors (SHRs) which are present in a heterocomplex with heat shock protein HSP90 and co-chaperones (e.g., immunophilins p23) (Echeverria PC & Picard D 2010). The ATP-bound form of HSP90 and chaperone-mediated conformational changes are required to keep SHRs in a ligand binding-competent state (McLaughlin SH et al. 2002; Pratt WB et al. 2008; Krukenberg KA et al. 2011).
In the absence of stress HSF1 is predominantly monomeric and is thought to be repressed in its inactive monomeric state by the following mechanisms: