Fig 1: FKBP51 links stress to secretory autophagy.a Results of automated literature mining of FKBP51 interactors in association to “autophagy”, “proteostasis” and “ubiquitin-proteasome system” (UPS) or none of them. b Western blotting of FKBP51 and SEC22B in GFP-tagged SEC22B co-IP (GFP-IP) and whole-cell extract (WCE) as control; c Western blotting of FKBP51 and SEC22B in FLAG-tagged FKBP51 co-IP (FLAG-IP) and WCE as control. d Western blotting of FKBP51, TRIM16, LC3B, and CTSD in FLAG-tagged FKBP51 co-IP (FLAG-IP) and WCE as control. e Western blotting for TRIM16, CTSD, and SEC22B in FLAG-tagged TRIM16 co-IP (FLAG-IP) and WCE as control performed in WT and FKBP5 KO SH-SY5Y cells. f Quantifications of e with n = 3 biologically independent samples. g Western blotting of TRIM16, CTSD, and SEC22B in FLAG-tagged TRIM16 co-IP (FLAG-IP) and WCE as control performed in cells treated with 100 nM dexamethasone or vehicle for 4 h. h Quantifications of g with n = 3 biologically independent samples. i Western blotting for FKBP51, SNAP23, SNAP29, STX3, and STX4 in FLAG-tagged FKBP51 co-IP (FLAG-IP) and WCE as control. j Western blotting of SEC22B, SNAP23, SNAP29, STX3, and STX4 in GFP-tagged SEC22B co-IP (GFP-IP) and WCE as control performed in WT and FKBP5 KO cells treated with 100 nM dexamethasone or vehicle for 4 h. k Quantifications of j with n = 3 biologically independent samples. b–k All experiments were performed in SH-SY5Y cells. l Schematic model of the interactions of FKBP51 in the secretory autophagy pathway. Unpaired, one-tailed t-tests were performed for all quantifications; ns not significant, **P < 0.01, ***P < 0.001. Data shown as mean ± s.e.m. Ab antibody, Fc fold change.