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. 2019 Sep 11;29:170–181. doi: 10.1016/j.molmet.2019.09.003

Figure 2.

Figure 2

Schematic representation of important metabolism-related cellular signaling cascades where FKBP51 was shown to play a decisive role (see main text for further details). (A) FKBP51 interacts with HSP90 and several steroid receptors (SR), including the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR) and thereby modulates SR ligand sensitivity, translocation and function. Among the genes that are regulated by glucocorticoids (GCs) via MR/GR activation is Fkbp5, thereby forming an ultra-short feedback loop. At the same time, FKBP5 has been shown to interact with other signaling pathways, thereby affecting cellular function in a cell-type specific manner [132], [133], [134]. (B) In fat tissue, FKBP51 was shown to affect PPARγ signaling and adipogenesis (not depicted) [73], [105]. In addition, an effect of UCP1 and consequently browning of white adipose tissue (WAT) has been postulated [4], [73]. (C) In muscle cells, FKBP51 interacts with AKT2 in the insulin signaling pathway, ultimately modulating cellular glucose uptake [4]. (D) In the brain, FKBP51 was shown to regulate autophagy via interaction with Beclin1 [56].