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Showing SH3GLB1 — BIF-1 is a alias.

SH3GLB1

Endophilin-B1 · UniProt Q9Y371

Length
365 aa
Mass
40.8 kDa
Annotated
2026-06-10
39 papers in source corpus 21 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SH3GLB1/Bif-1 (endophilin-B1) is a dual-domain membrane-remodeling protein that couples membrane curvature generation to the control of apoptosis, autophagy, and mitochondrial dynamics (PMID:16227588, PMID:17891140). Through its N-BAR domain it directly stimulates BAX-driven mitochondrial outer membrane permeabilization in a cardiolipin-dependent manner, heterodimerizing with Bax on mitochondria to promote BAX/BAK conformational activation, cytochrome c release, and caspase activation during intrinsic apoptosis (PMID:11259440, PMID:16227588, PMID:19074440); this pro-apoptotic interaction is suppressed by c-Src-mediated phosphorylation at tyrosine 80 (PMID:18474606). In autophagy, Bif-1 binds Beclin 1 via UVRAG (through its SH3 domain) to positively regulate the class III PI3-kinase VPS34 complex, while its membrane-binding/bending N-BAR domain drives Golgi membrane fission and the generation of Atg9-containing vesicles from a Rab11-positive reservoir together with Dynamin 2, supporting autophagosome formation (PMID:17891140, PMID:21068542, PMID:26980706). Bif-1 is required for mitophagy and autophagosome maturation (PMID:23287860, PMID:23680845), and under stress it translocates to mitochondria and binds prohibitin-2 via a C-terminal tryptophan-344, disrupting the prohibitin complex to induce OPA1 proteolysis and mitochondrial fragmentation (PMID:31126972). Beyond these core roles, Bif-1 mediates EGFR endocytic degradation (PMID:22785202), lipid catabolism and lipid-droplet clearance (PMID:26857140), and selective autophagic turnover of nicotinic acetylcholine receptors at the neuromuscular junction, the latter modulated by threonine-145 phosphorylation (PMID:24220501, PMID:27715385). Its loss promotes tumor development, linking impaired autophagy/mitophagy to genomic instability (PMID:17891140, PMID:23287860, PMID:23680845).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2001 High

    Established Bif-1's first molecular identity by showing it is a Bax-binding protein that can drive apoptosis, framing it as a pro-death regulator.

    Evidence Yeast two-hybrid cloning, Co-IP, immunofluorescence, and overexpression in IL-3-deprived FL5.12 cells

    PMID:11259440

    Open questions at the time
    • Did not show endogenous requirement
    • Mechanism of how Bif-1 promotes Bax conformational change unresolved
    • Domain requirements not defined
  2. 2005 High

    Demonstrated that endogenous Bif-1 is genetically required for Bax/Bak activation and MOMP, moving it from a sufficient overexpression effect to a necessary apoptotic mediator with tumor-suppressor implications.

    Evidence RNAi knockdown, Bif-1 KO MEFs, reciprocal Co-IP, apoptosis assays, and tumorigenesis assays

    PMID:16227588

    Open questions at the time
    • Indirect mechanism for Bak activation (no direct binding)
    • Biochemical mechanism of MOMP stimulation not reconstituted
  3. 2007 High

    Connected Bif-1 to autophagy by placing it in the UVRAG–Beclin1–VPS34 PI3KC3 complex and assigning distinct domain functions, defining its second major cellular role.

    Evidence Co-IP, domain-deletion mutants, siRNA, colocalization with Atg5/LC3, and KO mouse tumorigenesis

    PMID:17891140

    Open questions at the time
    • How N-BAR membrane activity feeds into PI3KC3 activation not mechanistically resolved
    • Site of autophagosome nucleation undefined
  4. 2008 High

    Resolved the biochemistry of Bif-1's pro-apoptotic action, proving the N-BAR domain directly stimulates BAX-mediated MOMP in a cardiolipin-dependent fashion separable from gross membrane remodeling.

    Evidence In vitro reconstitution with purified proteins and MOM-like liposomes plus N-BAR mutagenesis

    PMID:19074440

    Open questions at the time
    • Structural basis of N-BAR–BAX contact not defined
    • How cardiolipin requirement integrates with curvature generation unclear
  5. 2008 High

    Identified a phosphoregulatory switch by which c-Src phosphorylation at Y80 disrupts Bif-1–Bax binding, explaining how the apoptotic interaction is gated by survival signaling.

    Evidence Direct kinase assay, Y80 site-directed mutagenesis, Co-IP, and anoikis assay

    PMID:18474606

    Open questions at the time
    • Upstream signals controlling c-Src activity on Bif-1 not mapped
    • Structural effect of Y80 phosphorylation unknown
  6. 2010 Medium

    Extended the Bif-1/UVRAG/VPS34 sub-complex to receptor degradation and cytokinesis, broadening its membrane-trafficking roles beyond autophagosome formation.

    Evidence siRNA depletion of individual subunits with high-content microscopy and midbody localization

    PMID:20643123

    Open questions at the time
    • Direct role at midbody vs. indirect effect unresolved
    • Single lab, two approaches
  7. 2010 Medium

    Placed Bif-1 downstream of GSK-3β in an autophagy/cell-survival axis, identifying an upstream regulatory input to Bif-1 levels.

    Evidence GSK-3β chemical and siRNA inhibition with Bif-1 silencing and cell death assays

    PMID:20159967

    Open questions at the time
    • Mechanism linking GSK-3β to Bif-1 protein stabilization unknown
    • Whether regulation is transcriptional or post-translational unclear
  8. 2011 High

    Defined the membrane-fission mechanism of Bif-1 in autophagy, showing the N-BAR domain is required for starvation-induced Golgi fission and Atg9 vesicle generation.

    Evidence siRNA/KO loss-of-function, N-BAR mutant rescue, and live-cell imaging of Atg9 trafficking

    PMID:21068542

    Open questions at the time
    • How fission is spatially restricted to autophagy sites unclear
    • Partner fission machinery not yet defined at this stage
  9. 2012 Medium

    Implicated Bif-1 in EGFR endocytic degradation, showing its loss stalls cargo in Rab5 endosomes and sustains Erk signaling and migration.

    Evidence siRNA, EGFR degradation and Rab5/Rab7 colocalization assays, chemotaxis, and gefitinib rescue

    PMID:22785202

    Open questions at the time
    • Direct molecular role in endosome maturation vs. indirect effect unclear
    • Whether N-BAR or SH3 mediates this is undefined
  10. 2013 High

    Established Bif-1 as indispensable for mitophagy and autophagosome maturation, linking its loss to mitochondrial accumulation, DNA damage, and lymphomagenesis.

    Evidence Eμ-Myc Bif-1 KO/haploinsufficient mice, CCCP-treated PARK2 MEFs, EM, and mitochondrial mass assays

    PMID:23287860 PMID:23680845

    Open questions at the time
    • Mechanism by which Bif-1 promotes maturation step not defined
    • Selectivity for damaged mitochondria unexplained
  11. 2013 Medium

    Showed Bif-1 participates in selective autophagy of nicotinic acetylcholine receptors at the NMJ during muscle atrophy, extending its role to tissue-specific receptor turnover.

    Evidence In vivo denervation/fasting, ATG7 and TRIM63 KO mice, colocalization, and SQSTM1/LC3-II co-precipitation with CHRN

    PMID:24220501

    Open questions at the time
    • Direct Bif-1 interaction with CHRN cargo not shown
    • Recruitment mechanism to these vesicles unknown
  12. 2016 Medium

    Identified Dynamin 2 as the fission partner that cooperates with Bif-1 to generate Atg9 vesicles from a Rab11-positive reservoir, completing the membrane-fission machinery model.

    Evidence Co-IP, DNM2 GTPase inhibitor, KO rescue, and live-cell imaging with Rab11 colocalization

    PMID:26980706

    Open questions at the time
    • Stoichiometry/regulation of Bif-1–DNM2 complex unknown
    • How starvation enhances the interaction unresolved
  13. 2016 Medium

    Showed T145 phosphorylation tunes Bif-1's control of CHRN endocytic trafficking through RAB5 activity, adding a phosphoregulatory layer to its trafficking role.

    Evidence In vivo NMJ overexpression of T145E/T145A phosphomutants with vesicle tracking and RAB5 rescue

    PMID:27715385

    Open questions at the time
    • Kinase responsible for T145 phosphorylation not identified
    • Generalizability beyond NMJ unclear
  14. 2016 Medium

    Revealed a metabolic role for Bif-1 in lipid catabolism, with its loss reducing lipolysis and lipid-droplet clearance and promoting obesity.

    Evidence Bif-1 KO mice (aging and high-fat diet), adipose histology, lipolysis and liver lipid-droplet clearance assays

    PMID:26857140

    Open questions at the time
    • Whether lipid phenotype is autophagy-dependent not fully separated
    • Direct vs. systemic effects unresolved
  15. 2017 Medium

    Placed calpain (CAPNS1) upstream of Bif-1/Atg9 vesicle flux from Golgi, showing a calpain-cleavage-resistant Bif-1 mutant blocks autophagic flux.

    Evidence CAPNS1 siRNA, calpain-resistant Bif-1 point mutant, Atg9-Vps34 Co-IP, and Golgi/LC3 colocalization

    PMID:28302665

    Open questions at the time
    • Whether Bif-1 is a direct calpain substrate not definitively shown
    • Cleavage product function undefined
  16. 2019 High

    Defined a distinct mitochondrial inner-membrane mechanism in which stress-induced Bif-1 binds prohibitin-2 via W344 to disrupt the prohibitin complex, drive OPA1 proteolysis, and cause fragmentation, validated in renal ischemia/reperfusion injury.

    Evidence Co-IP, domain-deletion and W344 point mutant, Bif-1 KO MEFs and KO mice in a renal I/R model with OPA1 proteolysis assays

    PMID:31126972

    Open questions at the time
    • Trigger and machinery for Bif-1 mitochondrial translocation under stress not defined
    • How prohibitin disruption activates OPA1 protease unclear
  17. 2022 Medium

    Linked SUMO2 SUMOylation at K82 and ionizing radiation to Bif-1 association with mitochondrial proteins MFN1/2, TOM20, and Drp1, modulating radiation-induced mitophagy.

    Evidence Bioinformatic K82 prediction, Co-IP, confocal colocalization, and SH3GLB1 KO in cardiomyocytes and in vivo IR model

    PMID:35487252

    Open questions at the time
    • SUMOylation site only predicted bioinformatically
    • Functional consequence of K82 modification on each interaction not dissected
  18. 2018 Medium

    Showed alternative splicing by SRRM4 generates neural-specific Bif-1 isoforms with opposite apoptotic functions, indicating isoform identity reverses its pro-apoptotic activity in neuroendocrine prostate cancer.

    Evidence Transcriptome comparison, SRRM4 gain/loss, and isoform-specific apoptosis assays under camptothecin/UV

    PMID:29759485

    Open questions at the time
    • Molecular basis for anti-apoptotic switch in Bif-1b/c not defined
    • Domain differences between isoforms not mechanistically tested
  19. 2025 Low

    Tentatively extended Bif-1 to NOTCH2 signaling, with its depletion impairing N2ICD nuclear localization and glioblastoma growth.

    Evidence SH3GLB1 genetic depletion with N2ICD nuclear localization and in vivo tumor assays

    PMID:40639082

    Open questions at the time
    • Mechanism of how SH3GLB1 controls N2ICD nuclear localization undefined
    • No direct interaction shown
    • Single lab, limited methodological detail
  20. 2025 Low

    Identified SH3GLB1 as an in vitro fentanyl-binding protein, raising an unvalidated possible small-molecule interaction.

    Evidence Affinity-based protein profiling with a photoaffinity probe, click chemistry, and molecular docking (preprint)

    PMID:bio_10.1101_2025.02.20.634605

    Open questions at the time
    • No functional validation of the interaction
    • No mutagenesis or specificity controls
    • Physiological relevance unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • The signal and machinery that direct Bif-1 between its apoptotic, autophagic, mitophagic, and trafficking modes — and how its post-translational modifications (Y80, T145, K82, calpain cleavage) are coordinated — remain unresolved.
  • No unified model for how Bif-1 partitions among competing functions
  • Structural basis for partner selection (Bax vs. UVRAG vs. prohibitin-2) undefined
  • Upstream kinases/regulators of most modification sites unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005739 mitochondrion 3 GO:0005768 endosome 2 GO:0005794 Golgi apparatus 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 3 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
BAXBECN1DNM2DRP1MFN1PHB2SRCUVRAG
Complex memberships
UVRAG–Beclin1–VPS34 (PI3KC3) complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Bif-1 (SH3GLB1) was identified as a novel Bax-binding protein via yeast two-hybrid cloning. It contains an SH3 domain near its C-terminus and interacts with Bax as confirmed by coimmunoprecipitation and immunofluorescence. Overexpression of Bif-1 promotes Bax conformational change, caspase activation, and apoptotic cell death in FL5.12 cells following IL-3 deprivation. Yeast two-hybrid, coimmunoprecipitation, immunofluorescence, overexpression in FL5.12 cells The Journal of biological chemistry High 11259440
2005 Endogenous Bif-1 is required for conformational change of both Bax and Bak, cytochrome c release, and caspase-3 activation during intrinsic apoptosis. Bif-1 heterodimerizes with Bax on mitochondria in intact cells, and this interaction is enhanced by apoptosis induction and precedes Bax conformational change. While Bif-1 did not directly interact with Bak, it plays a regulatory role in Bak activation. RNAi knockdown in HeLa cells, Bif-1 knockout MEFs, coimmunoprecipitation, apoptosis assays (cytochrome c release, caspase-3 activation), soft-agar and nude-mouse tumorigenesis assays Molecular and cellular biology High 16227588
2007 Bif-1 interacts with Beclin 1 through UVRAG and functions as a positive mediator of the class III PI3-kinase (PI3KC3/VPS34). Both the BAR and SH3 domains are required for Bif-1 to activate PI3KC3 and induce autophagosome formation, while the SH3 domain alone is sufficient for binding to UVRAG. Upon nutrient deprivation, Bif-1 localizes to autophagosomes co-localizing with Atg5 and LC3. Loss of Bif-1 suppresses autophagosome formation and promotes spontaneous tumor development in mice. Coimmunoprecipitation, domain-deletion mutants, siRNA knockdown, immunofluorescence colocalization, Bif-1 knockout mouse tumorigenesis assay Nature cell biology High 17891140
2008 Bif-1 N-BAR domain stimulates BAX-driven mitochondrial outer membrane permeabilization (MOMP) and BAX conformational activation in a reconstituted system with purified proteins and MOM-like liposomes. This process requires physical interaction between Bif-1 N-BAR and BAX and the presence of cardiolipin. Large-scale membrane morphological rearrangements induced by Bif-1 N-BAR could be separated from functional BAX activation. DLP1/Drp1 caused global morphological changes in MOM-like liposomes but did not stimulate BAX-permeabilizing function. In vitro reconstitution with purified proteins and MOM-like liposomes, domain mutagenesis (N-BAR domain), cardiolipin-dependence assay, MOMP measurement The Journal of biological chemistry High 19074440
2008 c-Src kinase binds to Bif-1 and directly phosphorylates it on tyrosine 80. Src phosphorylation of Bif-1 suppresses its interaction with Bax, inhibiting Bax activation during anoikis. Apoptotic stimuli repress this phosphorylation event. Kinase assay, site-directed mutagenesis (Y80), coimmunoprecipitation, anoikis assay The Journal of biological chemistry High 18474606
2010 A specific PI3K-III sub-complex containing VPS15, VPS34, Beclin 1, UVRAG and BIF-1 (but not ATG14L) regulates both receptor degradation and cytokinesis. UVRAG and BIF-1 localize strongly to the midbody, supporting an unanticipated role of BIF-1 in cytokinesis. siRNA-mediated depletion of individual subunits, high-content microscopy-based assays for receptor degradation and cytokinesis, immunofluorescence localization to midbody Experimental cell research Medium 20643123
2010 GSK-3β inhibition results in elevation of Bif-1 protein levels, and silencing Bif-1 abrogates the GSK-3β-inhibition-induced autophagic response and necrotic cell death under serum starvation. This places Bif-1 downstream of GSK-3β in regulating autophagy and cell survival. GSK-3β chemical inhibitors and siRNA, Bif-1 siRNA silencing, cell death assays (morphology and biochemical markers), western blotting Journal of cell science Medium 20159967
2011 Bif-1 is required for Atg9 trafficking and fission of Golgi membranes during autophagy induction. Upon starvation, Atg9-positive membranes undergo tubulation and fragmentation to produce punctate structures positive for Rab5, Atg16L, and LC3. Loss of Bif-1 suppresses starvation-induced Golgi membrane fission and peripheral redistribution of Atg9. Bif-1 mutants lacking functional N-BAR domain regions (membrane binding/bending) fail to restore Golgi fission, Atg9 foci, and autophagosome formation in Bif-1-deficient cells. Loss-of-function (siRNA/KO), N-BAR domain mutants, live-cell fluorescence microscopy of Atg9 trafficking, Golgi morphology assays Autophagy High 21068542
2012 Bif-1 promotes EGFR endocytic degradation in breast cancer cells. Loss of Bif-1 delays EGFR degradation, sequesters internalized EGF in Rab5-positive endosomes, impairs Rab7 recruitment and activation, and alters intracellular pH and acidic vesicle localization. This results in sustained Erk1/2 activation and increased EGF-stimulated chemotactic cell migration. siRNA knockdown, EGFR degradation assay, Rab5/Rab7 colocalization by immunofluorescence, Erk1/2 activation by western blot, chemotaxis assay, EGFR inhibitor (gefitinib) rescue Cancer biology & therapy Medium 22785202
2013 Bif-1 is indispensable for autophagy-dependent clearance of damaged mitochondria (mitophagy). Loss of Bif-1 causes accumulation of ER-associated immature autophagosomes and suppresses autophagosome maturation. At the premalignant stage, allelic loss of Bif-1 increases mitochondrial mass, accumulation of DNA damage, and upregulation of Mcl-1, linking impaired mitophagy to chromosomal instability and apoptosis resistance during Myc-driven lymphomagenesis. Bif-1 KO/haploinsufficient mice with Eμ-Myc transgene, CCCP-treated PARK2-expressing MEFs, electron microscopy of autophagosome morphology, mitochondrial mass assays, immunoblotting for Mcl-1/Bcl-xl, caspase-3 activation assay Blood High 23287860 23680845
2013 SH3GLB1 (Bif-1) is present on endo/lysosomal carriers of nicotinic acetylcholine receptors (CHRN) at the neuromuscular junction during fasting-induced muscle atrophy, together with TRIM63 and SQSTM1, and these vesicles are surrounded by the autophagic marker MAP1LC3A in an ATG7-dependent fashion, indicating SH3GLB1 participates in selective autophagy-mediated CHRN turnover. In vivo mouse studies (denervation, fasting), ATG7 KO, TRIM63 KO, immunofluorescence colocalization, co-precipitation of SQSTM1/LC3-II with CHRN Autophagy Medium 24220501
2016 Bif-1 interacts with Dynamin 2 (DNM2) and this interaction is enhanced upon nutrient starvation. Bif-1 and DNM2 cooperatively induce the generation of Atg9-containing vesicles from a Rab11-positive reservoir. Inhibition of DNM2 GTPase activity causes accumulation of Atg9-positive tubular structures from this reservoir. Atg9 trafficking to the Rab11-positive reservoir is constitutive and independent of Bif-1, but membrane tubulation from the reservoir requires Bif-1. Coimmunoprecipitation, DNM2 GTPase inhibitor, live-cell fluorescence microscopy, Bif-1 KO rescue experiments, Rab11 colocalization Oncotarget Medium 26980706
2016 Threonine-145 phosphorylation of SH3GLB1 regulates CHRN (nicotinic acetylcholine receptor) endocytic trafficking at neuromuscular junctions. Phosphomimetic T145E mutant slows processing of endocytic CHRN vesicles, while phosphodeficient T145A augments it. Co-expression of RAB5 largely rescued the slow processing induced by T145E. SH3GLB1 phosphomutants alter the expression of RAB5 activity regulators. Overexpression of T145E/T145A phosphomutants in vivo at mouse NMJs, CHRN vesicle tracking, RAB5 co-expression rescue experiments, immunofluorescence Autophagy Medium 27715385
2016 Bif-1 deficiency reduces the basal rate of adipose tissue lipolysis, causes adipocyte hypertrophy, and attenuates fasting/refeeding-induced lipid droplet clearance in the liver, demonstrating a role for Bif-1 in regulating lipid catabolism and preventing obesity. Bif-1 loss also downregulates Atg9a and Lamp1 in adipose tissue. Bif-1 KO mice (aging and high-fat diet challenge), adipose tissue histology, lipolysis assays, liver lipid droplet clearance assay, western blotting for autophagy-lysosomal proteins Scientific reports Medium 26857140
2017 Calpain (activated via CAPNS1) enables dynamic flux of Atg9/Bif-1-containing vesicles from Golgi stacks toward the budding autophagosome. CAPNS1 depletion causes Atg9 and Bif-1 to remain in GM130-positive Golgi stacks, prevents Atg9 interaction with Vps34 and transferrin receptor, and causes LC3 body/Rab5 early endosome accumulation. A calpain-cleavage-resistant Bif-1 point mutant causes accumulation of p62 and LC3-II. CAPNS1 siRNA depletion, calpain-resistant Bif-1 point mutant overexpression, coimmunoprecipitation (Atg9-Vps34), immunofluorescence colocalization of Atg9/Bif-1 with Golgi/LC3 markers Biology open Medium 28302665
2018 The RNA splicing factor SRRM4 promotes alternative splicing of the Bif-1 gene, producing neural-specific isoforms Bif-1b and Bif-1c in treatment-induced neuroendocrine prostate cancer. The predominant variant Bif-1a is pro-apoptotic, whereas Bif-1b and Bif-1c are anti-apoptotic in PCa cells under camptothecin and UV treatment. Transcriptome comparison, SRRM4 overexpression and knockdown, isoform-specific apoptosis assays (camptothecin/UV treatment) EBioMedicine Medium 29759485
2019 Upon cell stress, Bif-1 translocates to mitochondria and binds prohibitin-2 via its C-terminus (specifically requiring tryptophan-344), resulting in disruption of the prohibitin complex and proteolytic inactivation/cleavage of the inner membrane fusion protein OPA1, promoting mitochondrial fragmentation and apoptosis. Bif-1 deficiency inhibits prohibitin complex disruption, OPA1 proteolysis, and mitochondrial fragmentation. In vivo, Bif-1 bound prohibitin-2 during renal ischemia/reperfusion injury, and Bif-1 KO protected against OPA1 proteolysis, fragmentation, and kidney injury. Coimmunoprecipitation, domain-deletion analysis, W344 point mutant, Bif-1 KO mice (renal ischemia/reperfusion model), MEFs, mitochondrial fractionation, OPA1 proteolysis assays Journal of the American Society of Nephrology : JASN High 31126972
2022 SUMO2-mediated SUMOylation of SH3GLB1 at lysine 82 is promoted by ionizing radiation, as shown by co-IP and laser confocal colocalization of SUMO2 and SH3GLB1. IR promotes interactions between SH3GLB1 and mitochondrial membrane proteins MFN1/2, TOM20, and Drp1. SH3GLB1 deficiency inhibits mitophagy activation and restores mitochondrial cristae. Bioinformatics prediction of SUMOylation site (K82), coimmunoprecipitation, laser confocal microscopy colocalization, SH3GLB1 KO in cardiomyocytes and in vivo IR model European journal of pharmacology Medium 35487252
2025 SH3GLB1 is required for the nuclear localization of the NOTCH2 intracellular domain (N2ICD) and NOTCH2 signaling activation in glioblastoma. Genetic depletion of SH3GLB1 impairs N2ICD nuclear localization, reduces tumorigenic potential, and impairs tumor growth in vivo. SH3GLB1 genetic depletion, N2ICD nuclear localization assay, in vivo tumor growth assay Biochemical and biophysical research communications Low 40639082
2025 Affinity-based protein profiling using a fentanyl-derived probe identified SH3GLB1 (endophilin-B1) as a protein that physically binds fentanyl in vitro across multiple species and tissue types, with molecular docking identifying putative binding sites. Affinity-based protein profiling with photoaffinity probe, click chemistry, molecular docking bioRxivpreprint Low bio_10.1101_2025.02.20.634605

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Bif-1 interacts with Beclin 1 through UVRAG and regulates autophagy and tumorigenesis. Nature cell biology 728 17891140
2005 Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis. Molecular and cellular biology 165 16227588
2010 A phosphatidylinositol 3-kinase class III sub-complex containing VPS15, VPS34, Beclin 1, UVRAG and BIF-1 regulates cytokinesis and degradative endocytic traffic. Experimental cell research 154 20643123
2001 Molecular cloning and characterization of Bif-1. A novel Src homology 3 domain-containing protein that associates with Bax. The Journal of biological chemistry 140 11259440
2011 Bif-1 regulates Atg9 trafficking by mediating the fission of Golgi membranes during autophagy. Autophagy 139 21068542
2009 Bif-1/endophilin B1: a candidate for crescent driving force in autophagy. Cell death and differentiation 113 19265852
2013 Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors. Autophagy 85 24220501
2010 GSK-3beta promotes cell survival by modulating Bif-1-dependent autophagy and cell death. Journal of cell science 70 20159967
2013 Bif-1 haploinsufficiency promotes chromosomal instability and accelerates Myc-driven lymphomagenesis via suppression of mitophagy. Blood 66 23287860
2008 Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements. The Journal of biological chemistry 55 19074440
2006 Decreased expression of tumour suppressor Bax-interacting factor-1 (Bif-1), a Bax activator, in gastric carcinomas. Pathology 54 16916719
2007 BARgaining membranes for autophagosome formation: Regulation of autophagy and tumorigenesis by Bif-1/Endophilin B1. Autophagy 42 18032918
2016 The Bif-1-Dynamin 2 membrane fission machinery regulates Atg9-containing vesicle generation at the Rab11-positive reservoirs. Oncotarget 39 26980706
2022 Canagliflozin Ameliorates NLRP3 Inflammasome-Mediated Inflammation Through Inhibiting NF-κB Signaling and Upregulating Bif-1. Frontiers in pharmacology 32 35418866
2019 Bif-1 Interacts with Prohibitin-2 to Regulate Mitochondrial Inner Membrane during Cell Stress and Apoptosis. Journal of the American Society of Nephrology : JASN 32 31126972
2008 Decreased expression of Bax-interacting factor-1 (Bif-1) in invasive urinary bladder and gallbladder cancers. Pathology 32 18752120
2012 Bif-1 suppresses breast cancer cell migration by promoting EGFR endocytic degradation. Cancer biology & therapy 29 22785202
2016 Bif-1 deficiency impairs lipid homeostasis and causes obesity accompanied by insulin resistance. Scientific reports 25 26857140
2015 IFNg-induced Irgm1 promotes tumorigenesis of melanoma via dual regulation of apoptosis and Bif-1-dependent autophagy. Oncogene 24 25619828
2008 SRC directly phosphorylates Bif-1 and prevents its interaction with Bax and the initiation of anoikis. The Journal of biological chemistry 24 18474606
2018 Roles of Alternative RNA Splicing of the Bif-1 Gene by SRRM4 During the Development of Treatment-induced Neuroendocrine Prostate Cancer. EBioMedicine 19 29759485
2016 Progress of endocytic CHRN to autophagic degradation is regulated by RAB5-GTPase and T145 phosphorylation of SH3GLB1 at mouse neuromuscular junctions in vivo. Autophagy 18 27715385
2022 SH3GLB1-related autophagy mediates mitochondrial metabolism to acquire resistance against temozolomide in glioblastoma. Journal of experimental & clinical cancer research : CR 17 35831908
2017 Calpain mobilizes Atg9/Bif-1 vesicles from Golgi stacks upon autophagy induction by thapsigargin. Biology open 15 28302665
2022 SUMO2-mediated SUMOylation of SH3GLB1 promotes ionizing radiation-induced hypertrophic cardiomyopathy through mitophagy activation. European journal of pharmacology 14 35487252
2013 Sh3glb1/Bif-1 and mitophagy: acquisition of apoptosis resistance during Myc-driven lymphomagenesis. Autophagy 13 23680845
2020 BIF-1 inhibits both mitochondrial and glycolytic ATP production: its downregulation promotes melanoma growth. Oncogene 11 32493957
2019 Bif-1/Endophilin B1/SH3GLB1 regulates bone homeostasis. Journal of cellular biochemistry 8 31243813
2009 Bif-1 and Bax expression in cutaneous Merkel cell carcinoma. Journal of cutaneous pathology 8 19125733
2012 Bif-1 is overexpressed in hepatocellular carcinoma and correlates with shortened patient survival. Oncology letters 6 22741005
2020 Loss of Concurrent Regulation of the Expression of BIF-1, BAX, and Beclin-1 in Primary and Metastatic Melanoma. Biochemistry. Biokhimiia 4 33202207
2016 Bif-1 promotes tumor cell migration and metastasis via Cdc42 expression and activity. Clinical & experimental metastasis 4 27730394
2025 Case Report: FGFR2 inhibitor resistance via PIK3CA and CDKN2A/B in an intrahepatic cholangiocarcinoma patient with FGFR2-SH3GLB1 fusion. Frontiers in oncology 2 40260297
2025 Hypoxia induced SH3GLB1 is required for NOTCH2 activation and glioblastoma development. Biochemical and biophysical research communications 1 40639082
2024 Bif‑1 inhibits activation of inflammasome through autophagy regulatory mechanism. Molecular medicine reports 1 38456519
2026 Revealing the Roles of the SH3GLB1-Hydrogen Peroxide Axis in Glioblastoma Multiforme Cells. Oncology research 0 41613801
2026 Bif-1 upregulates autophagy to improve nitrite tolerance of Litopenaeus vannamei by interacts with Prohibitin-2. International journal of biological macromolecules 0 42176919
2025 Inhibition of Bif-1 confers cardio-protection in myocardial infarction. American journal of physiology. Cell physiology 0 39982446
2023 Role of SH3GLB1 in the regulation of CD133 expression in GBM cells. BMC cancer 0 37525108

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