Affinage

FKBP8

Peptidyl-prolyl cis-trans isomerase FKBP8 · UniProt Q14318

Length
412 aa
Mass
44.6 kDa
Annotated
2026-06-09
83 papers in source corpus 47 papers cited in narrative 48 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FKBP8 (FKBP38) is a tail-anchored immunophilin of the outer mitochondrial membrane and ER that integrates apoptosis, organelle dynamics, autophagy, and growth signaling through a modular architecture of an FKBP-type PPIase domain, tandem TPR repeats, and an N-terminal LIR/LIRL region (PMID:12510191, PMID:15990872, PMID:28381481). Its peptidyl-prolyl isomerase activity is constitutively silent and switched on only upon heterodimerization with Ca2+/calmodulin, whereupon the activated enzyme binds Bcl-2 through a charged loop of its catalytic domain to promote apoptosis, an activity opposed by Hsp90, which binds the TPR domain via a MEEVD carboxylate clamp once the CaM-Ca2+ complex has formed and blocks the active site (PMID:15990872, PMID:17379601, PMID:17942410, PMID:22523079, PMID:28278223). In its non-activated state FKBP8 instead anchors Bcl-2/Bcl-xL to mitochondria to restrain apoptosis and protects Bcl-2 from caspase-3 cleavage, and this anti-apoptotic tethering is released by GTP-loaded Rheb (PMID:12510191, PMID:20048149, PMID:20139069). FKBP8 functions as an endogenous mTOR inhibitor by binding mTOR at the rapamycin-FKBP12 site; this inhibition is relieved by phosphatidic acid, which both displaces FKBP8 and allosterically activates the kinase, and the FKBP8–mTOR set point is tuned by its regulated turnover through signal peptide peptidase, RNF25/circSATB1, and ANKMY2/PHB1-dependent relocalization (PMID:17991864, PMID:21737445, PMID:30348988, PMID:33259040, PMID:39921520). At ER–mitochondria contact sites FKBP8 serves as the OMM tether for the ER protein PDZD8 and recruits the lipid-transfer protein BLTP1, governing contact-site architecture and mitochondrial lipid handling (PMID:40246839, PMID:38895210). Through its N-terminal LIR motif FKBP8 acts as a Parkin-independent mitophagy receptor that preferentially recruits LC3A and escapes degradation by translocating to the ER, while a distinct LIRL motif drives OPA1-dependent mitochondrial fragmentation, and its transmembrane domain supports VPS34-complex-dependent autophagy initiation (PMID:28381481, PMID:31908024, PMID:35090967). The TPR and PPIase domains additionally make FKBP8 a co-chaperone and quality-control hub: it promotes folding and trafficking of membrane proteins including CFTR and HERG, anchors the 26S proteasome to organellar membranes, stabilizes or destabilizes specific clients such as PHD2 and PRL-3, and is co-opted by viruses—assembling an Hsp90–NS5A complex required for HCV replication and targeting influenza M2 for lysosomal degradation (PMID:17024179, PMID:17353276, PMID:17573772, PMID:17569659, PMID:22030396, PMID:21320469, PMID:42212595). In vivo, FKBP8 is an essential cell-autonomous antagonist of Sonic hedgehog signaling acting downstream of Smoothened and upstream of Gli2, with loss causing neural tube and eye patterning defects (PMID:15105374, PMID:18590716, PMID:25077969).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 2003 High

    Established the founding biological role of FKBP8 by showing it anchors anti-apoptotic Bcl-2/Bcl-xL to the mitochondrial surface, defining it as an apoptosis regulator rather than a generic immunophilin.

    Evidence Co-IP, dominant-negative and RNAi loss-of-function with colocalization in mammalian cells

    PMID:12510191

    Open questions at the time
    • Did not resolve how the interaction is regulated
    • No structural basis for Bcl-2 binding
  2. 2004 High

    Revealed an unexpected developmental function by genetic knockout, placing FKBP8 as an essential antagonist of Sonic hedgehog signaling in neural patterning.

    Evidence Mouse knockout and in vivo neural tube patterning analysis

    PMID:15105374

    Open questions at the time
    • Molecular step in the Shh pathway not defined
    • Relationship to mitochondrial Bcl-2 function unclear
  3. 2005 High

    Solved how a constitutively inactive PPIase is activated, showing Ca2+/calmodulin binding switches on enzymatic activity that then directly engages Bcl-2 to promote apoptosis.

    Evidence In vitro PPIase assays, CaM-Ca2+ complex reconstitution, RNAi and inhibitor studies

    PMID:15733859 PMID:15990872

    Open questions at the time
    • Physiological trigger of Ca2+/CaM activation in cells not defined
    • How activation toggles between anti- and pro-apoptotic outputs unresolved
  4. 2005 Medium

    Refuted the earlier calcineurin-inhibition model and clarified that effects on calcineurin are indirect via Bcl-2, and showed presenilins regulate FKBP8/Bcl-2 stability and localization.

    Evidence In vitro phosphatase and NFAT reporter assays (negative); Co-IP, fractionation and knockin neurons

    PMID:15757646 PMID:15905180

    Open questions at the time
    • Negative calcineurin result from a single lab
    • Mechanism of presenilin-driven degradation not detailed
  5. 2006 High

    Defined FKBP8 as a host co-factor for HCV, showing its TPR domain assembles an Hsp90-NS5A ternary complex required for viral RNA replication and NS5A-mediated apoptosis suppression.

    Evidence Co-IP, siRNA, HCV replicon assays and yeast two-hybrid in hepatoma cells

    PMID:16844119 PMID:17024179

    Open questions at the time
    • How NS5A binding alters FKBP8 chaperone function not resolved
    • Quantitative affinity not yet measured at this stage
  6. 2007 High

    Proposed FKBP8 as the endogenous mTOR inhibitor displaced by GTP-Rheb, providing a candidate molecular link between Rheb and mTORC1 activation by nutrients and growth factors.

    Evidence Co-IP, in vitro mTOR kinase assay, GTP-dependent binding assays

    PMID:17991864

    Open questions at the time
    • Rheb-FKBP8 interaction subsequently contested
    • Stoichiometry and structural basis of mTOR inhibition unknown
  7. 2007 High

    Expanded the chaperone/quality-control repertoire by showing membrane-anchored FKBP8 stabilizes PHD2 via ubiquitin-independent proteasomal targeting, anchors the 26S proteasome to organelle membranes through its TPR domain, and promotes HERG channel trafficking.

    Evidence Y2H, GST pulldown, RNAi-plus-reconstitution, IP-MS, knockout MEFs, CHX chase and rescue assays

    PMID:17353276 PMID:17569659 PMID:17573772

    Open questions at the time
    • How a single protein both stabilizes and destabilizes clients not mechanistically unified
    • PPIase dispensability for PHD2 vs requirement for channel folding not reconciled
  8. 2007 High

    Defined the structural logic of Hsp90 regulation, showing Hsp90 binds the TPR domain only after CaM-Ca2+ binding and thereby blocks the PPIase active site to suppress pro-apoptotic activity, and mapped the CaM activation interface.

    Evidence Co-IP, in vitro binding and PPIase assays, NMR chemical shift perturbation, siRNA epistasis in neuroblastoma

    PMID:17379601 PMID:17942410 PMID:18036348

    Open questions at the time
    • In vivo balance of Hsp90 vs CaM occupancy not quantified
    • Cell-type specificity of the apoptotic switch unclear
  9. 2008 High

    Positioned FKBP8 precisely in the Shh pathway by genetic epistasis, acting downstream of Smoothened, upstream of Gli2 and dependent on the ciliary IFT subunit Kif3a, and linked loss to neural tube defects via protrudin.

    Evidence Mouse double-mutant epistasis, mosaic analysis, Y2H, phosphorylation analysis; SPR (Kd 82 nM) for NS5A and correlative fluorescence-EM

    PMID:18216108 PMID:18459960 PMID:18590716

    Open questions at the time
    • Direct molecular target of FKBP8 within the Shh/cilia axis not identified
    • Link between mitochondrial localization and ciliary signaling unexplained
  10. 2009 Medium

    Challenged the Rheb-effector model by failing to detect Rheb-FKBP8 interaction in three assays and assigning only a minor role to FKBP8 in mTORC1 activation.

    Evidence Multiple in vitro binding assays and cell-based mTORC1 activity assays (negative result)

    PMID:19222999

    Open questions at the time
    • Discrepancy with prior Science report not resolved
    • Single lab, conditions may differ from original study
  11. 2010 Medium

    Extended Rheb regulation to apoptosis and HCV biology, showing GTP-Rheb releases Bcl-xL from FKBP8, NS5A competes with mTOR for FKBP8 binding to activate mTOR, and FKBP8 protects Bcl-2 from caspase cleavage.

    Evidence GST pulldown, Co-IP, mTOR substrate phosphorylation, apoptosis and CHX-chase assays with binding-defective mutants

    PMID:20048149 PMID:20139069 PMID:20439463

    Open questions at the time
    • Reconciliation with the negative Rheb result still open
    • Quantitative contribution to physiological mTOR control unknown
  12. 2011 High

    Resolved part of the mTOR controversy by showing phosphatidic acid both displaces FKBP8 from mTOR and provides additional allosteric activation, and defined FKBP8 as a PPIase-dependent folding co-chaperone for CFTR.

    Evidence In vitro mTORC1 kinase and competition assays, PLD1/PA pathway validation; pulse-chase, PPIase and TPR mutants, surface electrophysiology

    PMID:21320469 PMID:21737445 PMID:22030396

    Open questions at the time
    • How PA-mediated displacement integrates with Rheb signaling unclear
    • PRL-3 degradation mechanism less defined
  13. 2012 High

    Provided atomic-level definition of the Bcl-2 interface, identifying the charge-sensitive beta5-alpha1 loop of the catalytic domain as the electrostatic Bcl-2 binding determinant.

    Evidence Heteronuclear NMR, peptide library assay, site-directed mutagenesis

    PMID:22523079

    Open questions at the time
    • Structure of the full FKBP8-Bcl-2 complex not solved
    • Relationship of this interface to PPIase catalysis not addressed
  14. 2013 Medium

    Identified a Ca2+/S100-dependent brake on the HCV complex, showing S100 proteins bind FKBP8 and disrupt both Hsp90 and NS5A interactions to suppress viral replication.

    Evidence GST/S-tag pulldown, SPR, HCV replicon replication assay

    PMID:23522085

    Open questions at the time
    • Physiological S100 levels needed for regulation unknown
    • Overlap with CaM regulation of the same surface not dissected
  15. 2017 High

    Recast FKBP8 as a Parkin-independent mitophagy receptor with an N-terminal LIR that preferentially recruits LC3A and a unique ability to escape degradation by translocating to the ER, and defined the TPR-Hsp90 MEEVD carboxylate-clamp interface structurally.

    Evidence Y2H, in vitro/in vivo pulldowns, LIR mutants, mitophagy flux assays; X-ray crystallography with MEEVD peptide and mutagenesis

    PMID:28278223 PMID:28381481

    Open questions at the time
    • Trigger and machinery for ER translocation not defined
    • Physiological mitophagy contribution debated across cell types
  16. 2017 Medium

    Demonstrated an ER-stress protective role in heart, showing cardiac FKBP8 loss causes protein aggregation and caspase-12-dependent apoptosis, while finding no mitophagy role in this context.

    Evidence Cardiac-specific knockout mice with TAC, IP, ER stress markers, caspase-12 inhibitor rescue (negative for mitophagy)

    PMID:29129702

    Open questions at the time
    • Cell-type basis for absent mitophagy not explained
    • Direct misfolded clients in cardiomyocytes not identified
  17. 2018 Medium

    Identified regulated FKBP8 turnover as a control node for mTOR and innate immunity, with signal peptide peptidase mediating its intramembrane proteolysis and FKBP8 negatively regulating RLR-VISA antiviral signaling.

    Evidence SILAC proteomics, Co-IP, CHX chase, proteasome inhibitors, xenograft; Y2H, reporter and ubiquitination assays

    PMID:30267576 PMID:30348988

    Open questions at the time
    • Physiological stimuli driving SPP cleavage unknown
    • Direct vs indirect effects on RLR components not fully separated
  18. 2019 High

    Distinguished a second N-terminal motif, the LIRL, as the OPA1-binding element driving Drp1-independent mitochondrial fragmentation under iron-depletion and hypoxic stress, separating fission from canonical LIR-mediated mitophagy.

    Evidence Functional screening, knockout MEF epistasis (Drp1, FIP200, BNIP3/NIX, OPA1), domain mutants, Co-IP with OPA1

    PMID:31908024

    Open questions at the time
    • Mechanism by which FKBP8-OPA1 binding promotes fission unclear
    • How LIR and LIRL functions are coordinated unknown
  19. 2020 Medium

    Connected FKBP8 to lipid metabolism and uncovered upstream localization control, with FKBP8 suppressing the mTOR/P70S6K/SREBP lipogenic axis and PHB1 governing its mitochondrial pool and mTOR association.

    Evidence Overexpression/knockdown with pathway readouts and HFD model; IP-MS, Co-IP and fractionation with PHB1 knockdown

    PMID:33259040 PMID:34900535

    Open questions at the time
    • Direct mechanism of lipid reduction beyond mTOR not defined
    • How PHB1 controls FKBP8 distribution mechanistically unknown
  20. 2022 High

    Diversified FKBP8 functions into autophagy initiation, epithelial barrier control and epigenetic regulation of Bcl-2 stability, including a PPIase-dependent MLCK1 interaction targetable by tacrolimus.

    Evidence VPS34 activity and autophagy flux assays with TM-domain mutants; in vitro binding, KO/dominant-negative cells, organoids, mouse and patient biopsies; demethylation and stability assays for KDM1A

    PMID:35090967 PMID:35537812 PMID:35970393

    Open questions at the time
    • How the same protein selects between LIR-driven mitophagy and TM-driven VPS34 autophagy unresolved
    • In vivo relevance of KDM1A-FKBP8 axis limited to cancer models
  21. 2024 High

    Established FKBP8 as the OMM tether for PDZD8 at ER-mitochondria contact sites, providing structural evidence that FKBP8 shapes contact-site architecture and mitochondrial morphology.

    Evidence BioID proximity proteomics, CRISPR endogenous tagging, cryo-electron tomography, CLEM and knockout epistasis

    PMID:38895210 PMID:40246839

    Open questions at the time
    • Functional output of PDZD8-FKBP8 tethering beyond morphology not fully defined
    • How tethering integrates with apoptotic and autophagic roles unknown
  22. 2025 Medium

    Linked FKBP8 contact-site tethering to lipid transport and turnover control, recruiting BLTP1 for mitochondrial lipid export and being degraded by RNF25/circSATB1 to relieve mTOR inhibition.

    Evidence Proximity proteomics, Co-IP, lipidomics, ROS and epistasis assays (preprint); Co-IP, ubiquitination and proteasome-inhibitor assays for RNF25

    PMID:39921520

    Open questions at the time
    • BLTP1 lipid-export finding is a preprint awaiting peer review
    • Directionality and selectivity of lipid transfer not fully established
  23. 2026 Medium

    Showed FKBP8 acts as an antiviral restriction factor against influenza A, using its TPR domain to bind M2 LIR and recruiting RAB7A/LAMP1 to drive lysosomal degradation of M2.

    Evidence AP-MS, Co-IP, overexpression/knockdown/knockout, lysosomal inhibitors, CHX chase and viral replication assays

    PMID:42212595

    Open questions at the time
    • Contrast with FKBP8's pro-viral HCV role not mechanistically reconciled
    • Single-lab finding without independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • How FKBP8 selects among its many mutually exclusive functions—pro- vs anti-apoptotic, mitophagy vs fission vs contact-site tethering, mTOR inhibition vs chaperone activity—through domain occupancy, localization and post-translational control remains the central open question.
  • No unified model linking domain state to functional output
  • In vivo physiological hierarchy of competing roles undetermined
  • Structural basis of the apoptotic switch in a cellular context unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016853 isomerase activity 3 GO:0044183 protein folding chaperone 3 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005739 mitochondrion 3 GO:0005783 endoplasmic reticulum 3
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 3 R-HSA-1266738 Developmental Biology 2
Partners
BCL2CALM1HSP90MAP1LC3AMTOROPA1PDZD8PHD2
Complex memberships
26S proteasome (membrane-anchored)FKBP8-CaM/Ca2+ complexFKBP8-PDZD8 ER-mitochondria tetherHsp90-FKBP8-NS5A ternary complex

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 FKBP8 (FKBP38) is localized to the outer mitochondrial membrane and functions to anchor Bcl-2 and Bcl-xL to mitochondria, inhibiting apoptosis. FKBP38 co-immunoprecipitates with Bcl-2 and Bcl-xL; dominant-negative mutants or RNAi-mediated depletion causes redistribution of Bcl-2/Bcl-xL away from mitochondria and promotes apoptosis. Co-immunoprecipitation, dominant-negative overexpression, RNAi, colocalization microscopy Nature cell biology High 12510191
2003 FKBP8-mediated cell size reduction downstream of TSC1/TSC2 was demonstrated; antisense knockdown of FKBP38 abolished TSC gene-dependent cell size effects, placing FKBP38 in the TSC/mTOR cell size control pathway. Antisense knockdown, microarray screen, cell size measurement Oncogene Medium 12894220
2004 Loss of FKBP8 in mice causes ectopic, ligand-independent activation of the Sonic hedgehog (SHH) signaling pathway in neural tissues, leading to expansion of ventral cell fates in the posterior neural tube and suppression of eye development, establishing FKBP8 as an essential antagonist of SHH signaling. Mouse knockout genetic analysis, in vivo neural patterning assays Development (Cambridge, England) High 15105374
2005 FKBP38 peptidyl-prolyl cis/trans isomerase (PPIase) activity is constitutively inactive but is activated upon formation of a heterodimeric complex with Ca2+/calmodulin. The activated complex directly binds Bcl-2 via the PPIase active site and regulates Bcl-2 function, promoting apoptosis in neuronal tissues. Biochemical PPIase activity assay, Ca2+/calmodulin complex formation, RNAi depletion, inhibitor studies The EMBO journal High 15990872
2005 FKBP38 interacts with Bcl-2 through the unstructured flexible loop of Bcl-2 (between helices 1 and 2), and this interaction can regulate phosphorylation within the Bcl-2 loop. Co-immunoprecipitation, deletion mutant mapping, biochemical interaction assays FEBS letters Medium 15733859
2005 FKBP38 does not directly inhibit calcineurin activity or physically interact with calcineurin in vitro or in vivo; FKBP38 indirectly affects calcineurin subcellular distribution through interaction with calcineurin ligands such as Bcl-2. This is a NEGATIVE result contradicting the earlier Shirane/Nakayama 2003 calcineurin inhibition claim. In vitro phosphatase activity assay, co-immunoprecipitation, NFAT reporter assay FEBS letters Medium 15757646
2005 Presenilins (PS1/2) interact with FKBP38 and form macromolecular complexes with Bcl-2. PS1/2 promote degradation of FKBP38 and Bcl-2 and sequester them in ER/Golgi compartments, thereby inhibiting FKBP38-mediated mitochondrial targeting of Bcl-2 and increasing susceptibility to apoptosis. Co-immunoprecipitation, subcellular fractionation, pulse-chase, RNAi, knockin mouse neurons Human molecular genetics High 15905180
2006 FKBP8 specifically interacts with HCV NS5A protein via FKBP8's tetratricopeptide repeat (TPR) domain. FKBP8 forms a ternary complex with Hsp90 and NS5A. siRNA knockdown of FKBP8 suppresses HCV RNA replication in hepatoma cells harboring an HCV replicon. Co-immunoprecipitation, siRNA knockdown, HCV replicon replication assay The EMBO journal High 17024179
2006 FKBP38-specific inhibitor DM-CHX inhibits the CaM/Ca2+-activated PPIase activity of FKBP38 with high selectivity (up to 80-fold higher affinity than for FKBP12). Neurotrophic FKBP ligands (GPI1046) preferentially inhibit FKBP38·CaM/Ca2+ over other neuroimmunophilins, linking FKBP38 PPIase inhibition to neuroprotective effects in a rat focal ischemia model. In vitro PPIase activity assay, competitive inhibition kinetics, rat focal cerebral ischemia model The Journal of biological chemistry Medium 16547004
2006 HCV NS5A inhibits apoptosis in Huh7 hepatoma cells specifically through interaction with FKBP38; RNAi depletion of FKBP38 abolishes the anti-apoptotic effect of NS5A. NS5A and FKBP38 co-localize in mitochondria and ER; the BH domain (aa 148-236) of NS5A mediates interaction with FKBP38. Yeast two-hybrid, in vitro GST pulldown, co-immunoprecipitation, RNAi, apoptosis assay FEBS letters Medium 16844119
2007 FKBP38 is identified as an endogenous inhibitor of mTOR that binds mTOR and inhibits its kinase activity similarly to the FKBP12-rapamycin complex. Rheb (GTP-bound form) directly interacts with FKBP38 and prevents FKBP38 association with mTOR in a GTP-dependent manner, thereby activating mTOR in response to growth factors and nutrients. Co-immunoprecipitation, in vitro kinase assay, GTPase-binding assay, overexpression/depletion of pathway components Science (New York, N.Y.) High 17991864
2007 FKBP8 specifically interacts with the HIF prolyl-4-hydroxylase PHD2 (but not PHD1 or PHD3) through N-terminal regions of both proteins. FKBP38 stabilization of PHD2 requires FKBP38's membrane anchoring; FKBP38 knockdown prolongs PHD2 protein stability, while reconstitution of FKBP38 expression reverses this effect. The PPIase activity of FKBP38 is dispensable for PHD2 regulation. Yeast two-hybrid, GST pulldown, co-immunoprecipitation, RNAi stable depletion with reconstitution, colocalization, cycloheximide chase Molecular and cellular biology High 17353276
2007 FKBP38 interacts via its three tandem TPR domains with the 26S proteasome (specifically with the S4 subunit of the 19S regulatory particle), anchoring the proteasome to the outer mitochondrial/ER membrane. Fkbp38-/- mouse embryonic fibroblasts show markedly reduced proteasome abundance and activity in membrane fractions. Immunoprecipitation/mass spectrometry, in vitro binding assay, Fkbp38 knockout MEFs, immunofluorescence Genes to cells : devoted to molecular & cellular mechanisms High 17573772
2007 FKBP38 promotes HERG potassium channel trafficking and maturation; FKBP38 co-immunoprecipitates and co-localizes with HERG, and siRNA knockdown of FKBP38 reduces HERG trafficking, while FKBP38 overexpression partially rescues a trafficking-deficient LQT2 mutant (F805C). Co-immunoprecipitation, siRNA knockdown, overexpression rescue, colocalization microscopy The Journal of biological chemistry Medium 17569659
2007 The TPR domain of FKBP38 interacts with the C-terminal domain of Hsp90, but only after FKBP38 has formed a complex with CaM-Ca2+. In the ternary Hsp90-FKBP38-CaM-Ca2+ complex, the active site of FKBP38 is blocked, preventing interaction with Bcl-2. Hsp90 thus acts as a negative regulator of FKBP38 pro-apoptotic activity. Co-immunoprecipitation, in vitro binding assays, PPIase activity assay The Journal of biological chemistry High 17379601
2007 CaM-Ca2+ activation of FKBP38 involves two distinct interaction sites: the C-terminal CaM-binding motif (residues Ser290-Asn313) binds the C-terminal CaM lobe in a Ca2+-dependent manner, while the N-terminal CaM lobe interacts with the catalytic FKBP38 domain in a Ca2+-independent manner; only the latter interaction activates FKBP38's enzymatic activity. NMR chemical shift perturbation, fluorescence spectroscopy, domain deletion mutants The Journal of biological chemistry High 17942410
2007 Hsp90 increases cell survival of neuroblastoma cells after apoptosis induction in a manner dependent on FKBP38; siRNA depletion of FKBP38 significantly reduces the anti-apoptotic effect of Hsp90, establishing that Hsp90 inhibits FKBP38-mediated pro-apoptotic activity in neuroblastoma cells. siRNA knockdown, apoptosis assays in neuroblastoma cells FEBS letters Medium 18036348
2008 HCV NS5A amino acid Val121 (conserved among all HCV genotypes) is a critical determinant for specific interaction with FKBP38; V121A substitution drastically impairs HCV replicon replication, and revertants restore Val121. FKBP8 partially co-localizes with NS5A in the cytoplasmic membranous web by correlative fluorescence-electron microscopy. Surface plasmon resonance (Kd = 82 nM), mutational analysis of NS5A, HCV replicon replication assay, correlative fluorescence-EM Journal of virology High 18216108
2008 FKBP8 disruption in mice activates Shh signaling cell-autonomously at a step downstream of Smoothened but upstream of Gli2 transcription factor, and this activation requires the kinesin-2 subunit Kif3a (IFT machinery/cilia). FKBP8 also indirectly promotes BMP signaling through its antagonism of Shh signaling. Genetic epistasis (double mutant analysis), mouse knockout, mosaic analysis Developmental biology High 18590716
2008 Fkbp38-/- mice exhibit spina bifida, disorganized neuroepithelium, increased apoptosis, and abnormal nerve fiber extension. FKBP38 interacts with protrudin (a membrane trafficking regulator), and protrudin is hyperphosphorylated in Fkbp38-/- brains, suggesting FKBP38 regulates protrudin-dependent membrane recycling and neurite outgrowth. Mouse knockout, yeast two-hybrid, phosphorylation analysis, histology Genes to cells : devoted to molecular & cellular mechanisms Medium 18459960
2009 Using three different in vitro assays, no interaction between Rheb and FKBP38 was detected, and FKBP38 plays only a very minor role in mTORC1 activation in cell biology experiments. This is a NEGATIVE result directly contradicting the Bai et al. 2007 Science paper. Multiple in vitro binding assays, cell-based mTORC1 activity assays FEBS letters Medium 19222999
2009 FKBP38 membrane anchoring via the C-terminal transmembrane domain is required for in cellulo interaction with PHD2 and for regulation of PHD2 protein abundance. FKBP38 mediates proteasomal interaction of PHD2 via a ubiquitin-independent proteasomal pathway. The minimal PHD2-binding domain of FKBP38 is a glutamate-rich sequence at the N-terminus, and PHD2 interacts with the MYND-type Zn2+ finger domain of FKBP38. PHD2 colocalizes with FKBP38 at the ER and mitochondria. Peptide array binding, fluorescence spectroscopy, FRET, biochemical fractionation, immunofluorescence, domain deletion analysis The Journal of biological chemistry High 19546213
2010 Rheb regulates FKBP38 interaction with Bcl-2 and Bcl-XL in a GTP-dependent manner in vitro and in response to amino acids and growth factors in cells. GTP-Rheb releases Bcl-XL from FKBP38, enabling Bcl-XL association with pro-apoptotic Bak, making cells more resistant to apoptosis. In vitro GST pulldown with Rheb variants, co-immunoprecipitation in cells, apoptosis assays The Journal of biological chemistry Medium 20048149
2010 HCV NS5A disrupts the mTOR-FKBP38 association in a manner dependent on NS5A-FKBP38 interaction, activating mTOR signaling. NS5A-mediated mTOR activation and apoptosis inhibition both require NS5A-FKBP38 binding. GST pulldown and Co-IP confirm NS5A directly competes with mTOR for FKBP38 binding. GST pulldown, co-immunoprecipitation, mTOR substrate phosphorylation assay, NS5A/FKBP38 mutant analysis The Journal of biological chemistry Medium 20439463
2010 FKBP38 protects Bcl-2 from caspase-3-dependent cleavage by direct interaction through the flexible loop of Bcl-2, which contains the caspase cleavage site. FKBP38 overexpression slows Bcl-2 degradation; knockdown accelerates it; the protective effect is reversed by caspase inhibitors or requires the Bcl-2-binding capacity of FKBP38. Co-immunoprecipitation, siRNA, cycloheximide chase, caspase inhibitor treatment, FKBP38 binding-defective mutants The Journal of biological chemistry Medium 20139069
2011 Phosphatidic acid (PA) activates mTORC1 by competing with FKBP38 for binding to mTOR at a site encompassing the rapamycin-FKBP12 binding domain. PA antagonizes FKBP38 inhibition of mTORC1 kinase activity in vitro and displaces FKBP38 from mTOR in cells. However, FKBP38 removal alone is insufficient to activate mTORC1; PA is additionally required for allosteric activation. In vitro mTORC1 kinase assay, competitive binding assay, RNAi, PLD1-dependent PA generation assay in cells The Journal of biological chemistry High 21737445
2011 FKBP38 promotes post-translational folding of CFTR in the ER via its PPIase active site. FKBP38 knockdown increases CFTR protein synthesis but inhibits post-translational folding, reducing steady-state CFTR levels, processing, and cell surface expression. Uncoupling FKBP38 from Hsp90 via TPR domain mutation modestly enhances CFTR maturation. Steady-state and pulse-chase analyses, siRNA knockdown, PPIase active site mutants, TPR domain mutants, surface electrophysiology The Journal of biological chemistry High 22030396
2011 FKBP38 interacts with and promotes degradation of PRL-3 (phosphatase of regenerating liver-3) via the proteasome pathway. The N-terminal region of FKBP38 is required for PRL-3 binding. FKBP38 overexpression reduces PRL-3 levels, while FKBP38 siRNA increases them. Yeast two-hybrid, co-immunoprecipitation, siRNA, proteasome inhibitor experiments, overexpression studies Biochemical and biophysical research communications Medium 21320469
2012 The charge-sensitive β5-α1 loop (Leu90-Ile96) of the FKBP38 catalytic domain, containing Asp92 and Asp94, is primarily responsible for Bcl-2 binding. The corresponding Bcl-2 binding epitope was identified via peptide library assay. Site-directed mutagenesis of key residues verified the electrostatic protein-protein interaction interface. Heteronuclear NMR spectroscopy, peptide library membrane assay, site-directed mutagenesis The Journal of biological chemistry High 22523079
2013 Ca2+/S100 proteins (S100A1, A2, A6, B, P) directly interact with FKBP8 in a Ca2+-dependent manner and inhibit FKBP8 interactions with both Hsp90 and NS5A, thereby also inhibiting HCV RNA replication. This defines a Ca2+-dependent regulatory mechanism suppressing the HCV NS5A-FKBP8-Hsp90 ternary complex. GST pulldown, S-tag pulldown, surface plasmon resonance, HCV replicon replication assay Liver international : official journal of the International Association for the Study of the Liver Medium 23522085
2014 ANKMY2 (a protein with ankyrin repeats and MYND Zn2+ finger) interacts with FKBP38 and acts downstream of FKBP38 in the Shh signaling pathway. Depletion of ANKMY2 decreases Shh signaling, while combined depletion of FKBP38 and ANKMY2 attenuates signaling, placing ANKMY2 downstream of FKBP38 as a positive regulator of Shh signaling. Proteomics, co-immunoprecipitation, siRNA epistasis in MEFs, zebrafish morpholino knockdown The Journal of biological chemistry Medium 25077969
2017 FKBP8 acts as a mitophagy receptor that binds LC3A via an N-terminal LIR motif. FKBP8 preferentially and strongly recruits lipidated LC3A to damaged mitochondria in a LIR-dependent manner, inducing Parkin-independent mitophagy when co-expressed with LC3A. Strikingly, FKBP8 escapes mitochondrial degradation during mitophagy by translocating away from mitochondria. Yeast two-hybrid, in vitro pull-down, in vivo co-immunoprecipitation, LIR mutant analysis, live fluorescence microscopy, mitophagy flux assays EMBO reports High 28381481
2017 Crystal structure of the FKBP8 TPR domain in complex with Hsp90 MEEVD-containing peptide reveals carboxylate clamp interactions critical for binding. Interactions upstream of the conserved MEEVD motif are required for tight Hsp90 binding. Mutation of Lys307 (in the carboxylate clamp) completely disrupts Hsp90 interaction. FKBP8 does not bind intact Hsp70. FKBP8-Hsp90 binding does not substantially affect Hsp90 ATPase activity. X-ray crystallography, mutagenesis, binding assays PloS one High 28278223
2017 FKBP8 knockout cardiomyocytes accumulate misfolded protein aggregates and show increased ER stress markers and caspase-12-dependent apoptosis under hemodynamic stress (TAC). FKBP8 is localized to ER and mitochondria in cardiomyocytes, interacting with Hsp90. FKBP8 knockdown had no effect on mitophagy in HEK293 cells or H9c2 myocytes (negative result for mitophagy in cardiac context). Cardiac-specific Fkbp8 knockout mice, TAC surgery, immunoprecipitation, immunofluorescence, ER stress marker analysis, caspase-12 inhibitor rescue Journal of molecular and cellular cardiology Medium 29129702
2018 Signal peptide peptidase (SPP) interacts with and co-localizes with FKBP8 in the ER and mediates intramembrane proteolysis-dependent degradation of FKBP8 in the cytosol via a proteasome pathway, thereby activating mTOR signaling. SILAC quantitative proteomics, co-immunoprecipitation, cycloheximide chase, proteasome inhibitor experiments, xenograft model Oncogene Medium 30348988
2018 FKBP8 negatively regulates innate antiviral RLR-VISA signaling by interacting with VISA (MAVS), RIG-I, and IRF3 during viral infection. FKBP8 overexpression attenuates IFN-β and NF-κB promoter activation and decreases IRF3 dimer formation. FKBP8 inhibits TBK1-IRF3 and VISA-TRAF3 complex formation and promotes polyubiquitination-mediated degradation of TBK1, RIG-I, and TRAF3. Yeast two-hybrid, co-immunoprecipitation, reporter assays, RNAi, ubiquitination assays Journal of medical virology Medium 30267576
2019 FKBP8 contains both an LIR motif and an LIR motif-like sequence (LIRL) at its N-terminus. The LIRL is essential for mitochondrial fragmentation and for FKBP8 binding to OPA1. FKBP8-induced mitochondrial fragmentation occurs independently of Drp1, FIP200, and BNIP3/NIX but requires OPA1. FKBP8 is recruited to sites of mitochondrial division during iron depletion stress and is required for mitochondrial fragmentation and mitophagy under hypoxic stress. Cell-based functional screening, FKBP8 knockdown and knockout MEFs, live microscopy, domain mutant analysis (LIR/LIRL), co-immunoprecipitation with OPA1 FASEB journal High 31908024
2020 FKBP8 overexpression decreases lipid content in vitro and in vivo via suppression of the mTOR/P70S6K/SREBPs pathway. FKBP8 overexpression/knockdown, mTOR substrate phosphorylation assay, lipid content assay, mouse HFD model Acta pharmaceutica Sinica. B Medium 34900535
2020 Prohibitin 1 (PHB1) specifically interacts with FKBP8 at mitochondria. PHB1 downregulation reduces FKBP8 levels in the mitochondrial fraction and increases FKBP8-mTOR interaction, linking mitochondrial PHB1 to mTOR pathway regulation via FKBP8 subcellular redistribution. Immunoprecipitation-mass spectrometry, co-immunoprecipitation, subcellular fractionation, PHB1 knockdown Frontiers of medicine Medium 33259040
2022 FKBP8 interacts with MLCK1 (myosin light chain kinase 1) via FKBP8's PPIase (tacrolimus-binding) domain. FKBP8 knockout or dominant-negative FKBP8 prevents TNF-induced MLCK1 recruitment to cell junctions and barrier loss. Tacrolimus blocks MLCK1-FKBP8 binding and reverses TNF-induced MLCK1 recruitment and barrier loss in vitro and in vivo. In vitro protein interaction assay, knockout/dominant-negative cell lines, intestinal organoids, mouse model, patient biopsy analysis, tacrolimus pharmacological intervention Gut High 35537812
2022 FKBP8 co-localizes with VPS34 complex members ATG14L and BECN1 and is necessary for VPS34 lipid kinase activity during starvation-induced autophagy. FKBP8 depletion abrogates autophagy activation by starvation; FKBP8 overexpression triggers autophagy. The transmembrane domain of FKBP8 (not the LIR) is required for this function and interaction with the VPS34 complex. FKBP8 is not found in completed autophagosomal vesicles. FKBP8 knockdown/overexpression, autophagy flux assays, colocalization microscopy, VPS34 activity assay, transmembrane domain mutant Biochimica et biophysica acta. Molecular cell research Medium 35090967
2022 KDM1A (lysine demethylase 1A) directly interacts with and demethylates FKBP8. Demethylation of FKBP8 by KDM1A enhances FKBP8 ability to stabilize BCL2. KDM1A cytoplasmic localization and stability are promoted by KAT8-mediated acetylation at lysine-117, which promotes FKBP8 demethylation and BCL2 accumulation. Co-immunoprecipitation, demethylation assay, protein stability assays, cancer cell lines and xenograft models The Journal of biological chemistry Medium 35970393
2024 FKBP8 is the tethering partner of the ER protein PDZD8 at ER-mitochondria contact sites (MERCS). Identified by unbiased proximity proteomics and validated by CRISPR-Cas9 endogenous tagging, cryo-electron tomography, and CLEM. FKBP8 overexpression narrows the ER-OMM distance; combined deletion of PDZD8 and FKBP8 is required for full loss of MERCS. PDZD8 enhances mitochondrial complexity in a FKBP8-dependent manner. Proximity proteomics (BioID), CRISPR-Cas9 endogenous tagging, cryo-electron tomography, correlative light-electron microscopy (CLEM), single molecule tracking, FKBP8/PDZD8 knockout analysis bioRxiv / Nature communications High 38895210 40246839
2025 FKBP8 recruits BLTP1 to ER-mitochondria contact sites via direct interaction, establishing a lipid export pathway from mitochondria. BLTP1 deficiency causes pathological accumulation of phosphatidic acid, phosphatidylglycerol, and cardiolipin, mitochondrial ROS elevation, and apoptosis. Depleting intramitochondrial lipid transfer proteins or CL synthesis enzymes prevents BLTP1-deficiency-induced apoptosis. Proximity proteomics, co-immunoprecipitation, lipidomics, mitochondrial ROS assay, genetic epistasis with lipid pathway knockdowns bioRxivpreprint Medium
2025 Phosphomimetic tau (at Ser-396/404 or Thr-231/Ser-235) inhibits oxidative stress-induced mitophagy and causes decreased levels of the mitophagy receptor FKBP8 (but not FUNDC1 or BNIP3) in response to paraquat. FKBP8 is normally trafficked to the ER during oxidative-stress-induced mitophagy, and disease-relevant tau impacts this trafficking, potentially through direct interaction. Immunoblot, subcellular fractionation, neuronal cell lines with tau mutants, paraquat-induced mitophagy assay PloS one Medium 39752365
2026 FKBP8 interacts with influenza A virus M2 protein via its TPR domain binding to the LIR sequence of M2 (high-affinity interaction). FKBP8 mediates lysosomal degradation of M2 by recruiting RAB7A and LAMP1 to form a FKBP8-RAB7A-LAMP1-M2 complex, inhibiting viral entry and replication. Affinity purification-MS, co-immunoprecipitation, FKBP8 overexpression/knockdown/knockout, lysosomal inhibitors (BafA1, CQ), cycloheximide assay, viral replication assays Autophagy Medium 42212595
2024 FKBP8 can initiate autophagosome biogenesis via two pathways: recruitment of the FIP200/ULK1 complex OR the WIPI-ATG13 complex, demonstrating hierarchical flexibility in autophagy initiation machinery. This was established by reconstitution experiments comparing FKBP8 with BNIP3/NIX, FUNDC1, BCL2L13, and TEX264. In vitro autophagy reconstitution, comparison of transmembrane autophagy receptors, genetic dissection of initiation complexes bioRxivpreprint Medium
2025 RNF25 E3 ubiquitin ligase mediates ubiquitination and degradation of FKBP8. CircSATB1 acts as a scaffold for the RNF25-FKBP8 complex, facilitating RNF25-mediated ubiquitylation of FKBP8 and its proteasomal degradation, thereby relieving FKBP8's inhibitory effect on mTOR signaling. Co-immunoprecipitation, ubiquitination assay, proteasome inhibitor experiments, FKBP8 knockdown/rescue Advanced science Medium 39921520

Source papers

Stage 0 corpus · 83 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 FKBP8 recruits LC3A to mediate Parkin-independent mitophagy. EMBO reports 351 28381481
2007 Rheb activates mTOR by antagonizing its endogenous inhibitor, FKBP38. Science (New York, N.Y.) 321 17991864
2003 Inherent calcineurin inhibitor FKBP38 targets Bcl-2 to mitochondria and inhibits apoptosis. Nature cell biology 270 12510191
2006 Hepatitis C virus RNA replication is regulated by FKBP8 and Hsp90. The EMBO journal 210 17024179
2005 Bcl-2 regulator FKBP38 is activated by Ca2+/calmodulin. The EMBO journal 117 15990872
2011 Phosphatidic acid activates mammalian target of rapamycin complex 1 (mTORC1) kinase by displacing FK506 binding protein 38 (FKBP38) and exerting an allosteric effect. The Journal of biological chemistry 108 21737445
2007 The peptidyl prolyl cis/trans isomerase FKBP38 determines hypoxia-inducible transcription factor prolyl-4-hydroxylase PHD2 protein stability. Molecular and cellular biology 94 17353276
2004 FKBP8 is a negative regulator of mouse sonic hedgehog signaling in neural tissues. Development (Cambridge, England) 93 15105374
2003 Cell size regulation by the human TSC tumor suppressor proteins depends on PI3K and FKBP38. Oncogene 87 12894220
2007 Co-chaperone FKBP38 promotes HERG trafficking. The Journal of biological chemistry 77 17569659
2006 The specific FKBP38 inhibitor N-(N',N'-dimethylcarboxamidomethyl)cycloheximide has potent neuroprotective and neurotrophic properties in brain ischemia. The Journal of biological chemistry 76 16547004
2005 Interaction of presenilins with FKBP38 promotes apoptosis by reducing mitochondrial Bcl-2. Human molecular genetics 74 15905180
2019 FKBP8 LIRL-dependent mitochondrial fragmentation facilitates mitophagy under stress conditions. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 64 31908024
2009 Hypoxia-inducible factor prolyl-4-hydroxylase PHD2 protein abundance depends on integral membrane anchoring of FKBP38. The Journal of biological chemistry 61 19546213
2008 FKBP8 cell-autonomously controls neural tube patterning through a Gli2- and Kif3a-dependent mechanism. Developmental biology 58 18590716
2008 A single-amino-acid mutation in hepatitis C virus NS5A disrupting FKBP8 interaction impairs viral replication. Journal of virology 52 18216108
2010 Hepatitis C virus NS5A activates the mammalian target of rapamycin (mTOR) pathway, contributing to cell survival by disrupting the interaction between FK506-binding protein 38 (FKBP38) and mTOR. The Journal of biological chemistry 51 20439463
2006 Hepatitis C virus non-structural protein NS5A interacts with FKBP38 and inhibits apoptosis in Huh7 hepatoma cells. FEBS letters 50 16844119
2007 Anchoring of the 26S proteasome to the organellar membrane by FKBP38. Genes to cells : devoted to molecular & cellular mechanisms 47 17573772
2010 Rheb GTPase controls apoptosis by regulating interaction of FKBP38 with Bcl-2 and Bcl-XL. The Journal of biological chemistry 45 20048149
2005 The flexible loop of Bcl-2 is required for molecular interaction with immunosuppressant FK-506 binding protein 38 (FKBP38). FEBS letters 45 15733859
2007 Mouse Fkbp8 activity is required to inhibit cell death and establish dorso-ventral patterning in the posterior neural tube. Human molecular genetics 43 18003640
2007 The Bcl-2 regulator FKBP38-calmodulin-Ca2+ is inhibited by Hsp90. The Journal of biological chemistry 42 17379601
2010 FKBP38 protects Bcl-2 from caspase-dependent degradation. The Journal of biological chemistry 41 20139069
2009 Reassessment of the role of FKBP38 in the Rheb/mTORC1 pathway. FEBS letters 39 19222999
2008 Regulation of apoptosis and neurite extension by FKBP38 is required for neural tube formation in the mouse. Genes to cells : devoted to molecular & cellular mechanisms 37 18459960
2022 Tacrolimus-binding protein FKBP8 directs myosin light chain kinase-dependent barrier regulation and is a potential therapeutic target in Crohn's disease. Gut 36 35537812
2017 FKBP8 protects the heart from hemodynamic stress by preventing the accumulation of misfolded proteins and endoplasmic reticulum-associated apoptosis in mice. Journal of molecular and cellular cardiology 35 29129702
2011 FKBP38 peptidylprolyl isomerase promotes the folding of cystic fibrosis transmembrane conductance regulator in the endoplasmic reticulum. The Journal of biological chemistry 35 22030396
2018 Signal peptide peptidase promotes tumor progression via facilitating FKBP8 degradation. Oncogene 34 30348988
2011 From cell death to viral replication: the diverse functions of the membrane-associated FKBP38. Current opinion in pharmacology 34 21514222
2017 The structure of FKBP38 in complex with the MEEVD tetratricopeptide binding-motif of Hsp90. PloS one 30 28278223
2007 A novel calmodulin-Ca2+ target recognition activates the Bcl-2 regulator FKBP38. The Journal of biological chemistry 29 17942410
2025 Mitochondrial complexity is regulated at ER-mitochondria contact sites via PDZD8-FKBP8 tethering. Nature communications 27 40246839
2017 Parkin-independent mitophagy-FKBP8 takes the stage. EMBO reports 27 28515082
2014 Mitochondria: FKBP38 and mitochondrial degradation. The international journal of biochemistry & cell biology 26 24657651
2022 FKBP8 is a novel molecule that participates in the regulation of the autophagic pathway. Biochimica et biophysica acta. Molecular cell research 25 35090967
2011 FKBP38-Bcl-2 interaction: a novel link to chemoresistance. Current opinion in pharmacology 25 21571591
2004 Fkbp8: novel isoforms, genomic organization, and characterization of a forebrain promoter in transgenic mice. Genomics 25 14667822
2021 Discovery of a potent FKBP38 agonist that ameliorates HFD-induced hyperlipidemia via mTOR/P70S6K/SREBPs pathway. Acta pharmaceutica Sinica. B 24 34900535
2022 Zexie Tang targeting FKBP38/mTOR/SREBPs pathway improves hyperlipidemia. Journal of ethnopharmacology 22 35151834
2022 Lysine demethylase KDM1A promotes cell growth via FKBP8-BCL2 axis in hepatocellular carcinoma. The Journal of biological chemistry 21 35970393
2014 Ca2+/S100 proteins inhibit the interaction of FKBP38 with Bcl-2 and Hsp90. The Biochemical journal 21 24295050
2005 A reassessment of the inhibitory capacity of human FKBP38 on calcineurin. FEBS letters 17 15757646
2016 Regulation of CLC-1 chloride channel biosynthesis by FKBP8 and Hsp90β. Scientific reports 16 27580824
2011 A charge-sensitive loop in the FKBP38 catalytic domain modulates Bcl-2 binding. Journal of molecular recognition : JMR 16 20140889
2011 The essential role of FKBP38 in regulating phosphatase of regenerating liver 3 (PRL-3) protein stability. Biochemical and biophysical research communications 16 21320469
2012 The FKBP38 catalytic domain binds to Bcl-2 via a charge-sensitive loop. The Journal of biological chemistry 15 22523079
2020 Prohibitin regulates mTOR pathway via interaction with FKBP8. Frontiers of medicine 14 33259040
2014 Role of the ANKMY2-FKBP38 axis in regulation of the Sonic hedgehog (Shh) signaling pathway. The Journal of biological chemistry 14 25077969
2013 Ca(2+) /S100 proteins regulate HCV virus NS5A-FKBP8/FKBP38 interaction and HCV virus RNA replication. Liver international : official journal of the International Association for the Study of the Liver 14 23522085
2016 FKBP8 interact with classical swine fever virus NS5A protein and promote virus RNA replication. Virus genes 12 26748656
2010 New structural aspects of FKBP38 activation. Biological chemistry 12 20707607
2007 Hsp90-mediated inhibition of FKBP38 regulates apoptosis in neuroblastoma cells. FEBS letters 11 18036348
2025 CircSATB1 Promotes Colorectal Cancer Liver Metastasis through Facilitating FKBP8 Degradation via RNF25-Mediated Ubiquitination. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 10 39921520
2023 Analysis of Dysferlin Direct Interactions with Putative Repair Proteins Links Apoptotic Signaling to Ca2+ Elevation via PDCD6 and FKBP8. International journal of molecular sciences 10 36902136
2008 Characterization of a Bcl-XL-interacting protein FKBP8 and its splice variant in human RPE cells. Investigative ophthalmology & visual science 10 18385096
2015 FKBP25 and FKBP38 regulate non-capacitative calcium entry through TRPC6. Biochimica et biophysica acta 9 26239116
2025 Tau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation. PloS one 8 39752365
2020 FKBP8 variants are risk factors for spina bifida. Human molecular genetics 8 32969478
2018 FKBP8 Enhances Protein Stability of the CLC-1 Chloride Channel at the Plasma Membrane. International journal of molecular sciences 8 30487393
2014 A critical role of noggin in developing folate-nonresponsive NTD in Fkbp8 -/- embryos. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery 8 24817375
2024 PDZD8-FKBP8 tethering complex at ER-mitochondria contact sites regulates mitochondrial complexity. bioRxiv : the preprint server for biology 7 38895210
2018 FKBP8 inhibits virus-induced RLR-VISA signaling. Journal of medical virology 7 30267576
2004 [Immunophilin FKBP38, an inherent inhibitor of calcineurin, targets Bcl-2 to mitochondria and inhibits apoptosis]. Nihon rinsho. Japanese journal of clinical medicine 7 14968553
2024 FKBP38 suppresses endometrial cancer cell proliferation and metastasis by inhibiting the mTOR pathway. Archives of biochemistry and biophysics 5 38218360
2017 Target of rapamycin FATC domain as a general membrane anchor: The FKBP-12 like domain of FKBP38 as a case study. Protein science : a publication of the Protein Society 5 29024217
2011 Temporal expression pattern of Fkbp8 in rodent cochlea. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 5 22178952
2024 GPX4 inhibits apoptosis of thyroid cancer cells through regulating the FKBP8/Bcl-2 axis. Cancer biomarkers : section A of Disease markers 4 38250761
2024 Tau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation. bioRxiv : the preprint server for biology 4 39026868
2015 Silencing FKBP38 gene by siRNA induces activation of mTOR signaling in goat fetal fibroblasts. Genetics and molecular research : GMR 4 26345900
2023 FKBP38 Regulates Self-Renewal and Survival of GBM Neurospheres. Cells 3 37947640
2017 NMR analysis of the backbone dynamics of the small GTPase Rheb and its interaction with the regulatory protein FKBP38. FEBS letters 3 29194576
2025 Nitrate maintains mitochondrial membrane integrity by increasing Sialin-FKBP8 granules via liquid-liquid-phase separation. Redox biology 2 41187501
2022 FKBP8, a new member of the PIK3C3/VPS34 complex. Autophagy reports 2 40396046
2024 FKBP38 deletion exacerbates ConA-induced hepatitis by promoting the immune response through the MCP-1/p38 pathway. International immunopharmacology 1 38996665
2012 Molecular Characterization and Tissue-specific Expression of a Novel FKBP38 Gene in the Cashmere Goat (Capra hircus). Asian-Australasian journal of animal sciences 1 25049623
2026 The sulfonamide anticancer agent indisulam enhances the chemosensitivity of gastric cancer cells by targeting FKBP8. The FEBS journal 0 41860182
2026 MicroRNA-663a upregulation upon ARID1A depletion promotes the growth and migration of esophageal cancer cells by targeting FKBP8. Translational cancer research 0 41969518
2026 FKBP8 inhibits influenza a virus infection by degrading viral M2 protein in lysosomes. Autophagy 0 42212595
2025 FKBP38 Alleviates Osteoarthritis Progression by Inhibiting Chondrocyte Senescence. Cartilage 0 41046448
2022 [Fkbp38 deletion induces premature ovarian insufficiency in mice by activating mTOR signaling and inducing granulosa cell apoptosis]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 36504053
2010 [Expression and antibody preparation of FKBP38 and its application]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 20584639

Missed literature

Know a paper Affinage missed for FKBP8? Flag it for the maintainers and the community.

No submissions yet.