Affinage

SH3GLB1

Endophilin-B1 · UniProt Q9Y371

Length
365 aa
Mass
40.8 kDa
Annotated
2026-04-28
38 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SH3GLB1 (Bif-1) is an N-BAR and SH3 domain-containing endophilin family protein that couples membrane remodeling to apoptosis, autophagy, and endosomal trafficking. In apoptosis, SH3GLB1 directly binds Bax on mitochondria to promote Bax/Bak conformational activation and mitochondrial outer membrane permeabilization in a cardiolipin-dependent manner, a function negatively regulated by c-Src phosphorylation at Y80; it also translocates to mitochondria under stress to bind prohibitin-2 via W344, disrupting the prohibitin complex and triggering OPA1 proteolysis and mitochondrial fragmentation (PMID:11259440, PMID:19074440, PMID:18474606, PMID:31126972). In autophagy, SH3GLB1 uses its SH3 domain to engage UVRAG within the Beclin 1–PI3KC3 complex to promote autophagosome nucleation, while its N-BAR domain drives Golgi membrane fission and generation of Atg9/Dynamin 2-containing vesicles required for autophagosome biogenesis and mitophagy (PMID:17891140, PMID:21068542, PMID:26980706, PMID:23287860). SH3GLB1 additionally facilitates endolysosomal EGFR degradation by promoting Rab7 recruitment to endosomes, and its loss leads to prolonged EGFR/ERK signaling, metabolic reprogramming with increased mitochondrial respiration and glycolysis, and impaired lipid catabolism (PMID:22785202, PMID:32493957, PMID:26857140).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2001 High

    The initial discovery that Bif-1 is a Bax-interacting protein established a direct molecular link between an endophilin-family BAR/SH3 protein and mitochondrial apoptosis.

    Evidence Yeast two-hybrid screen with Bax bait followed by co-immunoprecipitation, immunofluorescence, and overexpression apoptosis assays in IL-3-deprived cells

    PMID:11259440

    Open questions at the time
    • Endogenous stoichiometry and kinetics of Bif-1–Bax interaction unknown
    • Whether Bif-1 directly activates Bax or acts as a scaffold unresolved
    • Bak interaction status not addressed
  2. 2005 High

    Extending beyond overexpression, loss-of-function studies showed Bif-1 is required for both Bax and Bak conformational activation, cytochrome c release, and caspase-3 activation, establishing it as a non-redundant upstream regulator of intrinsic apoptosis.

    Evidence siRNA knockdown in HeLa and Bif-1 knockout MEFs with co-immunoprecipitation, mitochondrial fractionation, and caspase assays

    PMID:16227588

    Open questions at the time
    • Mechanism by which Bif-1 promotes Bak activation without direct binding unclear
    • Tissue-specific requirements not tested
  3. 2007 High

    Discovery that Bif-1 links to the Beclin 1–UVRAG–PI3KC3 autophagy complex via its SH3 domain revealed a second major function in autophagosome nucleation, distinct from its apoptotic role.

    Evidence Co-immunoprecipitation with domain deletion mapping, siRNA knockdown, fluorescence co-localization with Atg5 and LC3 upon nutrient deprivation

    PMID:17891140

    Open questions at the time
    • Whether Bif-1 membrane-bending activity is required for PI3KC3 activation versus autophagosome membrane supply not separated
    • Regulation of Bif-1–UVRAG interaction unknown
  4. 2008 High

    Two studies resolved regulatory and biophysical mechanisms: reconstitution showed Bif-1 N-BAR stimulates Bax-mediated liposome permeabilization in a cardiolipin-dependent manner, while c-Src phosphorylation at Y80 was identified as a negative switch that disrupts the Bif-1–Bax interaction during anoikis.

    Evidence Purified protein reconstitution on MOM-like liposomes with domain mutants (PMID:19074440); in vitro kinase assay with Y80 mutagenesis and anoikis assay (PMID:18474606)

    PMID:18474606 PMID:19074440

    Open questions at the time
    • Whether Y80 phosphorylation also regulates autophagy function not tested
    • Structural basis of cardiolipin requirement unresolved
    • Kinase(s) that dephosphorylate Y80 upon apoptosis not identified
  5. 2010 Medium

    Bif-1 was placed in a specific PI3KC3 sub-complex (with UVRAG, not ATG14L) that regulates endocytic receptor degradation and cytokinesis, revealing non-autophagic functions of this complex.

    Evidence Systematic siRNA depletion of PI3KC3 subunits with high-content microscopy for cytokinesis and receptor degradation phenotypes

    PMID:20643123

    Open questions at the time
    • Direct contribution of Bif-1 membrane bending to cytokinesis not tested
    • Whether midbody localization is dependent on UVRAG not determined
  6. 2011 High

    Structure-function analysis showed that Bif-1 N-BAR membrane-bending activity drives Golgi fission and Atg9 redistribution during starvation, mechanistically separating its membrane-remodeling role from PI3KC3 activation in autophagosome biogenesis.

    Evidence N-BAR domain mutants lacking membrane binding/bending in Bif-1 KO cells with live-cell imaging of Golgi fission and Atg9 puncta

    PMID:21068542

    Open questions at the time
    • Lipid specificity of N-BAR binding on Golgi membranes not characterized
    • Whether N-BAR acts alone or requires co-factors for fission unknown
  7. 2012 Medium

    Bif-1 was shown to promote EGFR endocytic degradation by facilitating Rab7 recruitment, establishing it as a regulator of endosome-to-lysosome trafficking beyond autophagy.

    Evidence siRNA knockdown with EGF trafficking imaging, Rab5/Rab7 co-localization, EGFR degradation kinetics, and gefitinib rescue of migration phenotype

    PMID:22785202

    Open questions at the time
    • Whether Bif-1 acts directly on Rab7 activation or indirectly via PI3KC3-UVRAG not resolved
    • Applicability to other receptor tyrosine kinases untested
  8. 2013 High

    Bif-1 was shown to be indispensable for mitophagy; its loss caused accumulation of immature autophagosomes at the ER and increased mitochondrial mass, linking its membrane-remodeling activity to organelle quality control and tumor suppression in a Myc-driven lymphoma model.

    Evidence Bif-1 KO and haploinsufficient mice crossed to Eμ-Myc transgenic model, electron microscopy, CCCP-induced mitophagy assay

    PMID:23287860

    Open questions at the time
    • Molecular mechanism of ER-to-autophagosome maturation arrest not identified
    • Whether Bif-1 directly senses mitochondrial damage unknown
  9. 2016 Medium

    Bif-1 was found to cooperate with Dynamin 2 in fission of Atg9-containing membranes from a Rab11-positive recycling endosome reservoir, defining the vesicle source and scission machinery for autophagosome membrane supply.

    Evidence Co-immunoprecipitation of Bif-1–DNM2, DNM2 GTPase inhibitor causing Atg9-positive tubule accumulation, live-cell imaging in Bif-1 KD cells

    PMID:26980706

    Open questions at the time
    • Direct biochemical reconstitution of Bif-1/DNM2-mediated membrane fission not performed
    • Whether other BAR proteins compensate partially not addressed
  10. 2016 Medium

    Bif-1 deficiency in mice impaired adipose tissue lipolysis and hepatic lipid droplet clearance, extending its autophagy/membrane-remodeling role to whole-body lipid metabolism.

    Evidence Bif-1 KO mice with adipose and liver metabolic phenotyping, Western blot for Atg9a and Lamp1

    PMID:26857140

    Open questions at the time
    • Cell-autonomous versus systemic contribution not separated
    • Lipid droplet autophagy mechanism not detailed
  11. 2017 Medium

    Calpain-dependent processing of Bif-1 was identified as a regulatory step for release of Atg9/Bif-1 vesicles from the Golgi during ER-stress-induced autophagy, adding a protease-based control layer.

    Evidence CAPNS1 siRNA, calpain-resistant Bif-1 mutant, Co-IP of Atg9–Vps34 interaction in depleted cells

    PMID:28302665

    Open questions at the time
    • Exact cleavage site and cleavage product identity not mapped
    • Whether calpain processing affects apoptotic function not tested
  12. 2018 Medium

    SRRM4-mediated alternative splicing was shown to generate neural-specific Bif-1 isoforms (Bif-1b/c) with anti-apoptotic properties, in contrast to the pro-apoptotic canonical Bif-1a, revealing isoform-specific functional switching in neuroendocrine prostate cancer.

    Evidence Whole-transcriptome sequencing, SRRM4 overexpression/knockdown, isoform-specific apoptosis assays in patient tumors and xenografts

    PMID:29759485

    Open questions at the time
    • Structural basis for isoform-specific apoptotic reversal not determined
    • Whether splice variants differ in autophagy function untested
  13. 2019 High

    A stress-induced mitochondrial translocation pathway was elucidated whereby Bif-1 binds prohibitin-2 via W344, disrupting the PHB1/PHB2 complex and triggering OPA1 proteolysis to drive mitochondrial fragmentation, providing a mechanistic link between Bif-1 and inner membrane dynamics.

    Evidence Reciprocal Co-IP, W344 point mutant, Bif-1 KO cells and mice, renal ischemia-reperfusion in vivo model with mitochondrial morphology analysis

    PMID:31126972

    Open questions at the time
    • Signal triggering Bif-1 mitochondrial translocation not identified
    • Whether PHB2 disruption also affects cristae-dependent apoptosis independently of OPA1 not tested
  14. 2020 Medium

    CRISPR knockout revealed that Bif-1 suppresses both mitochondrial respiration and glycolysis, identifying a metabolic tumor-suppressor function independent of its canonical apoptosis and autophagy roles.

    Evidence CRISPR/Cas9 KO in melanoma cells, Seahorse metabolic flux assays, in vitro and in vivo proliferation assays

    PMID:32493957

    Open questions at the time
    • Molecular mechanism by which Bif-1 suppresses respiration and glycolysis not identified
    • Whether this reflects a direct metabolic activity or indirect consequence of mitochondrial remodeling unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis of Bif-1 N-BAR selectivity for different organelle membranes, the identity of signals directing Bif-1 mitochondrial translocation, how Bif-1 directly suppresses mitochondrial metabolism, and whether the multiple post-translational modifications (Y80 phosphorylation, T145 phosphorylation, SUMOylation, calpain cleavage) act in a coordinated regulatory network.
  • No structural model of full-length Bif-1 or its complexes exists
  • Integrated PTM regulatory logic not tested
  • Isoform-specific functions in autophagy remain unexplored

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:0031410 cytoplasmic vesicle 3 GO:0005794 Golgi apparatus 2 GO:0005768 endosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-5357801 Programmed Cell Death 5 R-HSA-9612973 Autophagy 5 R-HSA-1430728 Metabolism 2 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
ATG9ABAXBECN1DNM2PHB2SRCUVRAG
Complex memberships
Beclin 1–UVRAG–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 a C-terminal SH3 domain, localizes to cytoplasm, and directly interacts with Bax as confirmed by co-immunoprecipitation and immunofluorescence. Overexpression of Bif-1 promotes Bax conformational change, caspase activation, and apoptotic cell death following IL-3 deprivation. Yeast two-hybrid, co-immunoprecipitation, immunofluorescence, overexpression apoptosis assay The Journal of biological chemistry High 11259440
2005 Bif-1 plays a regulatory role in apoptotic activation of both Bax and Bak. RNAi-mediated knockdown of Bif-1 in HeLa cells abrogated Bax and Bak conformational change, cytochrome c release, and caspase-3 activation. Bif-1 heterodimerizes with Bax on mitochondria, and this interaction is enhanced by apoptosis induction prior to Bax conformational change. Bif-1 does not directly interact with Bak. RNA interference, Bif-1 knockout MEFs, co-immunoprecipitation, mitochondrial fractionation, caspase activity assay Molecular and cellular biology High 16227588
2007 Bif-1 interacts with Beclin 1 through UVRAG and functions as a positive mediator of class III PI3-kinase (PI3KC3/Vps34). The SH3 domain of Bif-1 is sufficient for binding UVRAG, but both the BAR and SH3 domains are required to activate PI3KC3 and induce autophagosome formation. Upon nutrient deprivation, Bif-1 localizes to autophagosomes where it co-localizes with Atg5 and LC3. Loss of Bif-1 suppresses autophagosome formation. Co-immunoprecipitation, domain deletion mutants, siRNA knockdown, fluorescence microscopy, autophagosome formation assay Nature cell biology High 17891140
2008 Bif-1 N-BAR domain stimulates BAX-driven mitochondrial outer membrane permeabilization (MOMP) in a reconstituted system using purified proteins and MOM-like liposomes. This stimulatory effect requires physical interaction between Bif-1 N-BAR and BAX and depends on the presence of cardiolipin. Large-scale morphological membrane rearrangements by Bif-1 N-BAR could be separated from functional BAX activation. DLP1/Drp1 did not stimulate BAX permeabilizing function. In vitro reconstitution with purified proteins and MOM-like liposomes, liposome permeabilization assay, domain mutant analysis The Journal of biological chemistry High 19074440
2008 c-Src kinase directly binds to and phosphorylates Bif-1 on tyrosine 80. Src phosphorylation of Bif-1 suppresses the interaction between Bif-1 and Bax, thereby inhibiting Bax activation during anoikis. Apoptotic stimuli repress this phosphorylation event. In vitro kinase assay, co-immunoprecipitation, site-directed mutagenesis (Y80), anoikis apoptosis 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 degradative endocytic receptor downregulation and cytokinesis. BIF-1 and UVRAG localize strongly to the midbody during cytokinesis. siRNA depletion of individual subunits, high-content microscopy, cytokinesis and receptor degradation assays, subcellular localization Experimental cell research Medium 20643123
2010 GSK-3β inhibition results in elevation of Bif-1 protein levels. Silencing Bif-1 expression abrogates GSK-3β-inhibition-induced autophagic response and necrotic cell death under serum starvation, placing Bif-1 downstream of GSK-3β in regulating autophagy-dependent cell death. siRNA knockdown, chemical inhibitors, cell death assays (apoptosis/necrosis markers), autophagy monitoring Journal of cell science Medium 20159967
2011 Bif-1's N-BAR domain is required for membrane binding and bending activity and mediates fission of Golgi membranes during autophagy induction. Loss of Bif-1 or inhibition of the PI3KC3 complex II suppresses starvation-induced Golgi fission and peripheral redistribution of Atg9. N-BAR domain mutants lacking membrane binding/bending activity fail to restore Golgi fission, Atg9 puncta formation, or autophagosome formation. N-BAR domain mutants, fluorescence microscopy (live-cell), Bif-1 knockout/knockdown cells, Atg9 trafficking assay Autophagy High 21068542
2013 Bif-1 is indispensable for autophagy-dependent clearance of damaged mitochondria (mitophagy). Loss of Bif-1 results in accumulation of ER-associated immature autophagosomes and suppresses autophagosome maturation. Allelic loss of Bif-1 increases mitochondrial mass, accumulation of DNA damage, and upregulation of anti-apoptotic Mcl-1 in Myc-driven prelymphomatous cells. Bif-1 KO and haploinsufficient mice, Eμ-Myc transgenic lymphoma model, electron microscopy, mitophagy assay (CCCP treatment), flow cytometry Blood High 23287860
2013 SH3GLB1 (Bif-1) is present on endolysosomal carriers containing nicotinic acetylcholine receptors (CHRN) in skeletal muscle neuromuscular junctions. SH3GLB1-positive CHRN vesicles are surrounded by autophagic marker LC3 in an ATG7-dependent fashion, placing SH3GLB1 in selective autophagy-mediated CHRN turnover regulated by TRIM63. Co-immunoprecipitation, immunofluorescence co-localization, ATG7 knockout mice, denervation model Autophagy Medium 24220501
2016 Bif-1 interacts with Dynamin 2 (DNM2) and this interaction is enhanced upon nutrient starvation. Bif-1 and DNM2 cooperatively mediate fission of Atg9-containing membranes from a Rab11-positive reservoir during autophagy. Inhibition of DNM2 GTPase activity results in accumulation of Atg9-positive tubular structures. Atg9 trafficking to the Rab11 reservoir is Bif-1-independent, but membrane tubulation from this reservoir requires Bif-1. Co-immunoprecipitation (Bif-1–DNM2 interaction), DNM2 GTPase inhibitor, fluorescence microscopy, Bif-1 KD cells, live-cell imaging Oncotarget Medium 26980706
2016 Threonine-145 phosphorylation of SH3GLB1 regulates CHRN endocytic trafficking at the neuromuscular junction. Phosphomimetic T145E SH3GLB1 slows processing of endocytic CHRN vesicles, while phosphodeficient T145A augments it. Co-expression of RAB5 largely rescues the slowed processing induced by T145E. Phosphomutants alter expression of RAB5 activity regulators without changing RAB5 co-localization with CHRN vesicles. Overexpression of T145E and T145A phosphomutants, RAB5 co-expression rescue, in vivo neuromuscular junction imaging Autophagy Medium 27715385
2016 Bif-1 deficiency reduces basal adipose tissue lipolysis and impairs fasting/refeeding-induced lipid droplet clearance in the liver, promoting adipocyte hypertrophy and obesity. Bif-1 loss downregulates Atg9a and Lamp1 expression in adipose tissue, linking its membrane-curvature function to lipid catabolism. Bif-1 knockout mice, adipose tissue lipolysis assay, hepatic lipid droplet clearance assay, Western blotting Scientific reports Medium 26857140
2017 Calpain (CAPNS1-dependent) is required for dynamic flux of Atg9/Bif-1 vesicles from Golgi stacks toward autophagosomes upon thapsigargin-induced autophagy. CAPNS1 depletion causes Atg9 and Bif-1 to remain in GM130-positive Golgi stacks. A Bif-1 point mutant resistant to calpain processing leads to accumulation of endogenous p62 and LC3-II. Atg9 fails to interact with Vps34 in CAPNS1-depleted cells. CAPNS1 siRNA depletion, calpain-resistant Bif-1 point mutant, co-immunoprecipitation (Atg9-Vps34), fluorescence microscopy Biology open Medium 28302665
2018 SRRM4 promotes alternative RNA splicing of the Bif-1 gene to produce neural-specific variants Bif-1b and Bif-1c in treatment-induced neuroendocrine prostate cancer. Bif-1a (predominant in adenocarcinoma) is pro-apoptotic, while Bif-1b and Bif-1c are anti-apoptotic under camptothecin and UV treatment. Whole transcriptome sequencing, SRRM4 overexpression/knockdown, isoform-specific apoptosis assays, patient tumor samples and xenografts EBioMedicine Medium 29759485
2019 Upon cell stress, Bif-1 translocates to mitochondria and binds prohibitin-2 via its C-terminus (specifically via tryptophan-344), causing disruption of the prohibitin complex and proteolytic inactivation of the inner membrane fusion protein OPA1, leading to mitochondrial fragmentation and apoptosis. Bif-1 deficiency or W344 mutation prevents prohibitin-2 binding, OPA1 proteolysis, and mitochondrial fragmentation. Co-immunoprecipitation, domain deletion analysis, W344 point mutation, Bif-1 KO cells and mice, renal ischemia-reperfusion model, mitochondrial morphology analysis Journal of the American Society of Nephrology High 31126972
2020 BIF-1 inhibits both mitochondrial respiration and glycolytic ATP production. CRISPR/Cas9 knockout of BIF-1 in melanoma cells results in increased mitochondrial respiration, metabolic acidification, and ATP production, promoting higher proliferation rates in vitro and in vivo, independent of effects on apoptosis and autophagy. CRISPR/Cas9 knockout, Seahorse metabolic assay, in vitro and in vivo proliferation assays Oncogene Medium 32493957
2022 SUMO2 SUMOylates SH3GLB1 at position K82 (predicted and validated by co-IP and confocal co-localization). Ionizing radiation promotes the interaction between SUMO2 and SH3GLB1, and SH3GLB1 interacts with mitochondrial membrane proteins MFN1/2, TOM20, and Drp1 upon IR, mediating mitophagy activation. SH3GLB1 deficiency inhibits mitophagy and restores mitochondrial cristae. Co-immunoprecipitation, laser confocal microscopy, SH3GLB1 KO cells, mitophagy assay, bioinformatics prediction of SUMOylation site European journal of pharmacology Low 35487252
2012 Bif-1 promotes EGFR endocytic degradation. Loss of Bif-1 sequesters internalized EGF in Rab5-positive endosomes, delays EGFR trafficking to lysosomes, impairs Rab7 recruitment and activation to EGF-positive vesicles, and prolongs ERK1/2 activation. Bif-1 suppression increases chemotactic cell migration in an EGFR-dependent manner. siRNA knockdown, fluorescence microscopy (Rab5, Rab7, EGF trafficking), EGFR degradation assay, ERK phosphorylation assay, migration assay with gefitinib rescue Cancer biology & therapy Medium 22785202
2025 SH3GLB1 is required for nuclear localization of the NOTCH2 intracellular domain (N2ICD) and NOTCH2 pathway activation in glioblastoma cells under hypoxia. SH3GLB1 is transcriptionally induced by HIF-2A under hypoxic conditions, and its genetic depletion reduces tumorigenic potential and impairs tumor growth in vivo. Genetic depletion (siRNA/shRNA), nuclear fractionation, NOTCH2 signaling assay, in vivo xenograft, HIF-2A transcription factor binding analysis Biochemical and biophysical research communications Low 40639082

Source papers

Stage 0 corpus · 38 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 725 17891140
2005 Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis. Molecular and cellular biology 164 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
2011 Bif-1 regulates Atg9 trafficking by mediating the fission of Golgi membranes during autophagy. Autophagy 139 21068542
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 139 11259440
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 84 24220501
2010 GSK-3beta promotes cell survival by modulating Bif-1-dependent autophagy and cell death. Journal of cell science 69 20159967
2013 Bif-1 haploinsufficiency promotes chromosomal instability and accelerates Myc-driven lymphomagenesis via suppression of mitophagy. Blood 63 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 38 26980706
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
2022 Canagliflozin Ameliorates NLRP3 Inflammasome-Mediated Inflammation Through Inhibiting NF-κB Signaling and Upregulating Bif-1. Frontiers in pharmacology 29 35418866
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 17 27715385
2022 SH3GLB1-related autophagy mediates mitochondrial metabolism to acquire resistance against temozolomide in glioblastoma. Journal of experimental & clinical cancer research : CR 16 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
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