Affinage

BCL2L10

Bcl-2-like protein 10 · UniProt Q9HD36

Length
204 aa
Mass
23.2 kDa
Annotated
2026-06-09
60 papers in source corpus 26 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BCL2L10 (Boo/Diva/Bcl-B/Nrh) is an anti-apoptotic BCL-2 family protein that restrains the mitochondrial (intrinsic) death pathway and integrates apoptosis with autophagy and Ca2+ signaling (PMID:11278245, PMID:11689480). It localizes to intracellular membranes through its hydrophobic C-terminal transmembrane domain, which is required for organelle association and full anti-apoptotic activity (PMID:9878060, PMID:11278245), and blocks cytochrome c release, mitochondrial membrane potential collapse, and caspase-3 activation while sparing death-receptor (TNFα/CD95) signaling (PMID:11689480, PMID:11557035). Its defining biochemical feature is selectivity: it binds and suppresses Bax but not Bak, recognizing the BH3 domain of Bax through a structurally defined BH3-binding pocket, and engages a restricted set of BH3-only partners (Bim and Bik) (PMID:12921534, PMID:23235460). A crystal structure of the Bcl-B:Bim complex reveals an unstructured loop inserted between helices α5 and α6 that distinguishes it from other family members, and this region harbors an evolutionarily acquired calcium-binding motif (PMID:23235460, PMID:21705382). Beyond direct effector neutralization, BCL2L10 acts at the ER and mitochondria-associated membranes, where its BH4 domain binds the IP3 receptor to suppress ER Ca2+ release, an activity antagonized by dephosphorylated IRBIT during apoptotic stress to promote ER-mitochondria Ca2+ transfer (PMID:27995898, PMID:29330143). It additionally suppresses autophagy by binding the BH3 domain of Beclin-1 and displacing PI3KC3 (PMID:22498477, PMID:30696802), and dampens mitophagy by binding and inhibiting phospho-Parkin (PMID:30635551). BCL2L10 abundance is tightly controlled by K48-linked polyubiquitination at K128 (with K119/K120) targeting it for proteasomal degradation, while the chaperone-like ubiquilins UBQLN1 and UBQLN4 selectively bind and stabilize the protein (PMID:23563182, PMID:22233804, PMID:34245648). The protein is not a passive survival factor: the nuclear receptor Nur77/TR3 binds Bcl-B and converts it from anti- to pro-apoptotic (PMID:17227826), and its survival function is exploited in cancer, where STAT3-driven transcription confers resistance to cisplatin and ABT-737—to which BCL2L10 is intrinsically insensitive (PMID:33396645, PMID:22875003). In oocytes, BCL2L10 associates with TPX2 and regulates Aurora kinase A to support meiotic spindle assembly and the metaphase I-to-II transition (PMID:27753540, PMID:19439730).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1999 High

    Established BCL2L10 as a membrane-associated anti-apoptotic BCL-2 family member that physically engages the apoptosome, defining its first mechanistic foothold in the death pathway.

    Evidence Co-IP, pulldown and subcellular fractionation showing Boo-Apaf-1/caspase-9 complex formation and membrane localization via the C-terminus

    PMID:9878060

    Open questions at the time
    • Whether Apaf-1 binding is direct or bridged was not resolved
    • Did not define which BH domains mediate effector versus apoptosome interactions
  2. 2001 High

    Defined the domain architecture and pathway placement, showing BCL2L10 blocks the mitochondrial pathway upstream of caspases but not death-receptor signaling, and requires its BH4 and TM domains.

    Evidence Co-IP, GST pulldown, cytochrome c/caspase-3/membrane-potential readouts and domain deletion across transfection systems

    PMID:11278245 PMID:11557035 PMID:11566354 PMID:11689480

    Open questions at the time
    • Pro- versus anti-apoptotic behavior in different cell contexts left unreconciled
    • Structural basis for Bax-not-Bak selectivity not yet established
  3. 2003 High

    Resolved the molecular basis of Bax-selective inhibition, showing recognition of the Bax BH3 domain through a defined binding pocket whose mutation abolishes function.

    Evidence BH3-swap chimeras, alanine scanning, and structure-based pocket mutagenesis with apoptosis readouts

    PMID:12921534

    Open questions at the time
    • Did not explain why Bak BH3 is excluded structurally
    • No co-structure provided at this stage
  4. 2007 High

    Showed BCL2L10 is not a unidirectional survival factor: Nur77/TR3 binding converts it to a pro-apoptotic effector, and identified NM23-H2 as a negative regulator of its abundance.

    Evidence Endogenous Co-IP, RNAi epistasis and fluorescence polarization (Nur77); yeast two-hybrid, Co-IP and siGN (NM23-H2)

    PMID:17227826 PMID:17532299

    Open questions at the time
    • Conformational basis of the anti-to-pro-apoptotic switch unknown
    • NM23-H2 mechanism of down-regulation not defined as direct
  5. 2008 High

    Comparative profiling cemented Bax-over-Bak selectivity as a distinguishing property among anti-apoptotic family members and revealed insensitivity to ABT-737.

    Evidence Three independent binding assays (Co-IP, GST pulldown, fluorescence polarization with BH3 peptides) plus apoptosis assays; HIP1R interaction by Y2H/Far-Western

    PMID:18178565 PMID:19255499

    Open questions at the time
    • HIP1R-induced BAK-dependent death mechanism incompletely placed
    • Therapeutic consequence of ABT-737 insensitivity not yet tested
  6. 2009 Medium

    Extended BCL2L10 function beyond apoptosis to oocyte biology, linking it to microtubule/TCTP association and meiotic progression.

    Evidence Co-IP, immunofluorescence, neutralizing-antibody and dsRNA microinjection with spindle/MPF readouts in oocytes

    PMID:19439730 PMID:19551325

    Open questions at the time
    • Whether the meiotic role is mechanistically distinct from apoptosis suppression unclear
    • Single-lab oocyte system; direct partners of the spindle role undefined at this point
  7. 2011 Medium

    Identified an evolutionarily acquired calcium-binding motif in the α5-α6 interhelical region, foreshadowing a Ca2+-related function.

    Evidence Site-directed mutagenesis, truncation constructs and phylogenetic analysis with biochemical readouts

    PMID:21705382

    Open questions at the time
    • Functional consequence of Ca2+ binding not demonstrated in cells
    • Limited functional validation in the report
  8. 2012 High

    Defined the proteostatic control of BCL2L10 and expanded its function to autophagy suppression and a defined structural fold.

    Evidence Mass spectrometry, site-specific ubiquitin mutagenesis, linkage-specific antibodies, cycloheximide chase (K128 K48-ubiquitination; UBQLN1 stabilization); Co-IP/autophagy flux (Beclin-1); 1.9 Å crystal structure with Bim

    PMID:22233804 PMID:22498477 PMID:22875003 PMID:23235460 PMID:23563182

    Open questions at the time
    • The E3 ligase for K128 ubiquitination not identified
    • How ubiquilin stabilization and ubiquitin-driven degradation are coordinated unresolved
  9. 2016 High

    Established the ER/MAM Ca2+ axis, showing BCL2L10 inhibits the IP3 receptor and is antagonized by dephosphorylated IRBIT to license apoptosis, and linked it to meiotic spindle assembly via TPX2/Aurora A.

    Evidence Co-IP, MAM fractionation, Ca2+ imaging and phosphorylation assays (IRBIT); Co-IP, co-localization, RNAi and kinase activity assay (TPX2/Aurka)

    PMID:27753540 PMID:27995898

    Open questions at the time
    • How IRBIT phosphorylation state is sensed by BCL2L10 mechanistically unclear
    • Aurora A regulation shown by RNAi correlation, not direct enzymatic mechanism
  10. 2018 High

    Confirmed BH4-dependent IP3R inhibition at the ER as an anti-apoptotic mechanism with therapeutic relevance, as BH4 mimetic peptides suppress tumor growth.

    Evidence Confocal localization, Co-IP, BH4-deletion mutagenesis, Ca2+ release assays and in vitro/in vivo tumor models

    PMID:29330143

    Open questions at the time
    • Whether IP3R inhibition and effector sequestration act independently in tumors unclear
    • Specificity of BH4 mimetics for BCL2L10 over related proteins not addressed
  11. 2019 Medium

    Connected BCL2L10 to mitophagy and autophagy regulation in tissue contexts, showing it inhibits phospho-Parkin and displaces PI3KC3 from Beclin-1.

    Evidence Co-IP with phospho-Parkin, siRNA/overexpression with mitophagy and apoptosis assays (HSCs); Co-IP, ELISA and autophagy flux (Beclin-1/PI3KC3 in hepatoma)

    PMID:30635551 PMID:30696802

    Open questions at the time
    • Whether Parkin inhibition is via direct dephosphorylation or steric block unresolved
    • Single-lab, tissue-specific findings; generality across cell types untested
  12. 2021 Medium

    Placed BCL2L10 in cancer drug-resistance circuits, defining STAT3 transcriptional control, UBQLN4-mediated stabilization, and a BOK interaction driving persister-cell phenotypes.

    Evidence ChIP/reporter/mutagenesis and siRNA with drug-sensitivity readouts (STAT3, melanoma); Co-IP and genetic screening (UBQLN4); Co-IP and MOMP/EMT assays (BOK, lung cancer)

    PMID:33396645 PMID:34245648 PMID:39996719

    Open questions at the time
    • Direct versus indirect nature of BOK-driven sublethal MOMP unclear
    • How STAT3, ubiquilin stabilization, and degradation jointly set BCL2L10 levels in tumors not integrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • The E3 ubiquitin ligase that drives K48/K128 turnover, the structural mechanism of the Nur77-induced anti-to-pro-apoptotic switch, and how the apoptotic, Ca2+, autophagic, and meiotic roles are coordinated in vivo remain unresolved.
  • No identified E3 ligase for BCL2L10 degradation
  • No structural model of the pro-apoptotic conformation
  • No integrated in vivo model linking the multiple cellular functions

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140313 molecular sequestering activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005739 mitochondrion 3 GO:0005783 endoplasmic reticulum 2 GO:0005829 cytosol 2
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 3 R-HSA-8953897 Cellular responses to stimuli 2
Partners
APAF1BAXBECN1BIMBOKIRBITITPR1UBQLN1
Complex memberships
Bcl-B:Bim complexIRBIT-Bcl2l10 complex at MAMsTPX2-containing meiotic spindle complex

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Boo (BCL2L10) interacts with Apaf-1 and forms a multimeric protein complex with Apaf-1 and caspase-9; pro-apoptotic Bak and Bik disrupt the Boo-Apaf-1 association. Boo also binds three distinct regions of Apaf-1. Co-immunoprecipitation, pulldown assays, transfection-based apoptosis assays The EMBO journal High 9878060
1999 Boo (BCL2L10) localizes to intracellular membranes via its hydrophobic C-terminus and inhibits apoptosis; it homodimerizes and heterodimerizes with other Bcl-2 family members. Subcellular fractionation, co-immunoprecipitation, transfection-based apoptosis assays The EMBO journal High 9878060
2001 Bcl-B (BCL2L10) contains BH1, BH2, BH3, BH4, and a C-terminal transmembrane domain; it binds Bcl-2, Bcl-XL, and Bax but NOT Bak. It suppresses Bax-induced but not Bak-induced apoptosis. Deletion of the TM domain impairs association with intracellular organelles and diminishes anti-apoptotic function. Co-immunoprecipitation, GST pulldown, transient transfection apoptosis assays, domain deletion mutagenesis The Journal of biological chemistry High 11278245
2001 Bcl2-L-10 blocks apoptosis in the mitochondrial death pathway (preventing cytochrome C release, caspase-3 activation, and mitochondrial membrane potential collapse) but does not block TNFα-induced (death receptor) apoptosis. Both the BH4 domain and transmembrane domain are necessary for its anti-apoptotic function. Transfection assays, cytochrome C release measurement, caspase-3 activation assay, mitochondrial membrane potential assay, domain deletion mutagenesis Human molecular genetics High 11689480
2003 Bcl-B selectively binds Bax over Bak via the BH3 domain of Bax; chimeric Bak containing Bax's BH3 domain bound Bcl-B whereas chimeric Bax containing Bak's BH3 domain did not. Alanine-scanning of Bax BH3 and structure-based mutations in Bcl-B's BH3-binding pocket (L86A and R96Q) abolished Bax binding and apoptosis suppression, confirming binding-dependent suppression mechanism. BH3-swap chimeric mutant co-immunoprecipitation, alanine-scanning mutagenesis, structure-based mutagenesis of BH3-binding pocket, transient transfection apoptosis assays The Biochemical journal High 12921534
2007 Nuclear receptor Nur77/TR3 selectively binds Bcl-B among anti-apoptotic Bcl-2 family members and converts Bcl-B from anti-apoptotic to pro-apoptotic. Endogenous Bcl-B associates with endogenous Nur77 in RPMI 8226 myeloma cells, and RNAi knockdown of Bcl-B demonstrated dependence on Bcl-B for Nur77-induced apoptosis. Co-immunoprecipitation of endogenous proteins, RNAi knockdown, fluorescence polarization binding assay, peptide treatment assays Blood High 17227826
2007 NM23-H2 interacts with Diva/BCL2L10 (requiring the transmembrane domain of Diva) and co-localizes in cytoplasm. NM23-H2 overexpression down-regulates Diva protein level; NM23-H2 knockdown restores Diva expression and increases Diva-mediated apoptotic activity. Yeast two-hybrid, co-immunoprecipitation, siRNA knockdown, subcellular co-localization Biochemical and biophysical research communications Medium 17532299
2008 Bcl-B shows strong preference for binding and suppressing Bax over Bak, in contrast to Bcl-2, Bcl-XL, Bcl-W, and Bfl-1 which bind both. Bcl-B is not targeted by ABT-737 due to low affinity. Co-immunoprecipitation, GST pulldown, fluorescence polarization with synthetic BH3 peptides, transient transfection apoptosis assays The Journal of biological chemistry High 18178565
2009 HIP1R interacts with BCL2L10 (requiring both ANTH and THATCH domains of HIP1R); HIP1R overexpression induces cell death dependent on BAK (not BAX), associated with mitochondrial membrane potential loss and caspase-9 activation, and augments BCL2L10-caspase-9 association. Yeast two-hybrid, co-immunoprecipitation, Far-Western analysis, domain deletion, caspase-9 activation assay, mitochondrial membrane potential assay Cellular physiology and biochemistry Medium 19255499
2009 BCL2L10 protein is associated with the microtubule binding protein TCTP (translationally controlled tumor protein) and with mitochondria in oocytes, with stage-specific redistribution along the pericortical regulatory ooplasm. Neutralization of BCL2L10 accelerated oocyte death. Co-immunoprecipitation, immunofluorescence, neutralizing antibody treatment, subcellular fractionation Journal of molecular medicine Medium 19551325
2009 Bcl2l10 RNAi in mouse germinal vesicle oocytes causes metaphase I arrest with spindle and chromosome abnormalities; Bcl2l10 affects maturation-promoting factor activity but not MAPK activity at the MI-MII transition. Microinjection of dsRNA, immunofluorescence for spindle/chromosomes, MPF and MAPK activity assays Biology of reproduction Medium 19439730
2012 BCL2L10 (BCLb) protein stability is regulated by Ubiquilin1 (Ubqln1), which specifically interacts with BCLb (but not other anti-apoptotic BCL2 family members), stabilizes BCLb protein, promotes its monoubiquitination on multiple lysine residues, and relocalizes it to the cytosol. Immunoaffinity purification, mass spectrometry, cycloheximide chase, co-immunoprecipitation, ubiquitination assays Proceedings of the National Academy of Sciences of the United States of America High 22233804
2012 Bcl-B is polyubiquitinated at steady state via K48-linked chains; K128 is the primary acceptor site (confirmed by mass spectrometry and linkage-specific antibodies), with K119 and K120 as additional sites. Ubiquitination targets Bcl-B for proteasomal degradation and controls its anti-apoptotic capacity. A lysineless Bcl-B mutant shows 5-fold higher protein expression than wild-type. Mutagenesis (lysine substitutions), mass spectrometry, linkage-specific ubiquitin antibodies, proteasome inhibition, cycloheximide chase Oncogene High 23563182
2012 Bcl-B interacts with the BH3 domain of BECN1 (Beclin-1) and inhibits autophagy; Bcl-B overexpression reduces autophagy triggered by various stimuli while Bcl-B knockdown triggers autophagic cell death dependent on LC3, BECN1, and ATG5. Co-immunoprecipitation, autophagy flux assays, siRNA knockdown, overexpression studies Autophagy Medium 22498477
2012 Bcl-B has high-affinity interactions with Bim and Bik BH3-only proteins only; it does not bind other BH3-only proteins with high affinity. Crystal structure of Bcl-B:Bim complex resolved to 1.9 Å reveals an insertion of an unstructured loop between helices α5 and α6 distinguishing Bcl-B from other family members. X-ray crystallography (1.9 Å resolution), fluorescence polarization binding assays, cell-based apoptosis assays Cell death & disease High 23235460
2012 Bcl-B is not targeted by ABT-737 (low affinity), in contrast to Bcl-2, Bcl-xL, and Bcl-w. Noxa, but not Bim, Puma, or truncated Bid, can overcome Bcl-B-mediated resistance to ABT-737. Inducible expression system, cell-based apoptosis assays with BH3-only protein expression, drug treatment experiments Cell death & disease Medium 22875003
2016 IRBIT interacts with Bcl2l10 and they additively inhibit IP3R in the physiological state. Upon apoptotic stress, IRBIT is dephosphorylated and becomes an inhibitor of Bcl2l10. The IRBIT-Bcl2l10 complex associates in mitochondria-associated membranes (MAMs); IRBIT promotes ER-mitochondria contact and facilitates Ca2+ transfer to mitochondria to promote apoptosis by inhibiting Bcl2l10. Co-immunoprecipitation, IP3R activity assays, phosphorylation assays, subcellular fractionation (MAM isolation), Ca2+ imaging, IRBIT knockdown eLife High 27995898
2016 Bcl2l10 co-localizes on meiotic spindles with Tpx2 and Aurora kinase A (Aurka); Bcl2l10 is present in the same complex as Tpx2. Bcl2l10 RNAi decreases Tpx2 and Aurka expression while increasing phospho-Aurka, resulting in decreased Aurka catalytic activity, disrupted MTOC formation, and impaired meiotic spindle assembly. Co-immunoprecipitation, immunofluorescence co-localization, RNAi, kinase activity assay Cell cycle Medium 27753540
2018 Nrh/BCL2L10 localizes to the endoplasmic reticulum and makes BH4 domain-dependent interactions with the ligand-binding domain of IP3R (type 1/3 Ca2+ channel), negatively regulating ER-Ca2+ release to mediate anti-apoptosis. Disrupting Nrh/IP3R complexes with BH4 mimetic peptides inhibits breast cancer cell growth in vitro and in vivo. Immunofluorescence/confocal localization, co-immunoprecipitation, BH4-domain deletion mutagenesis, Ca2+ release assays, in vitro and in vivo tumor growth assays Cancer research High 29330143
2019 BCL-B binds phospho-Parkin directly and inhibits its phosphorylation, thereby suppressing mitophagy in hepatic stellate cells. BCL-B knockdown increases both mitophagy and apoptosis in HSCs, while BCL-B overexpression has the opposite effects. Co-immunoprecipitation of BCL-B with phospho-Parkin, siRNA knockdown, overexpression, mitophagy assays, apoptosis assays Experimental & molecular medicine Medium 30635551
2019 BCL2L10 interacts with BECN1 (Beclin-1) in hepatoma cells; this interaction reduces the association between BECN1 and PI3KC3, thereby suppressing autophagy via the PI3K/AKT signaling pathway. Co-immunoprecipitation, ELISA, immunofluorescence co-localization, autophagic flux monitoring (LC3B-II/P62), PI3K/AKT pathway analysis Aging Medium 30696802
2020 BCL2L10 expression is driven by STAT3-mediated transcription; functional STAT3 responsive elements were identified in the BCL2L10 promoter. BCL2L10 confers resistance to cisplatin, dacarbazine, and ABT-737 in melanoma; genetic and pharmacological inhibition of BCL2L10 sensitized cells to cisplatin and ABT-737. Reporter assays, site-directed mutagenesis of STAT3 binding sites, ChIP analysis, siRNA knockdown, pharmacological inhibition Cancers Medium 33396645
2021 UBQLN4 interacts with and stabilizes BCL2L10, preventing mesothelioma cell apoptosis in response to DNA damage. UBQLN4 itself is a substrate of ATM kinase. Co-immunoprecipitation, functional genetic screening, apoptosis assays Molecular oncology Medium 34245648
2011 Human BCL2L10 has evolved a calcium-binding motif in its α5-α6 interhelical region through acquisition of critical negatively charged residues. Deletion of the N-terminal extension had no significant functional impact in HeLa cells, but the interhelical region mutation affects function. Site-directed mutagenesis, truncation constructs, biochemical assays, phylogenetic analysis Molecular biology and evolution Medium 21705382
2001 Human Boo/Diva (BCL2L10) is not exclusively localized to mitochondria before apoptosis induction; EGFP-Boo/Diva translocates to mitochondria during vincristine-induced apoptosis. Overexpression of human Boo/Diva promoted cell death in HeLa and 293 cells. Bcl-XL interacts with Boo but cannot protect cells from Boo/Diva-induced cell death. GFP-fusion live imaging, co-immunoprecipitation, overexpression apoptosis assays Biochimica et biophysica acta Medium 11566354
2001 In human glioma cells, Diva/Boo (BCL2L10) inhibits apoptosis induced by CD95 ligand or chemotherapeutic drugs, and interferes with apoptotic signaling downstream of cytochrome c release but upstream of caspase activation, consistent with inhibition of the apoptosome/Apaf-1. Overexpression assays, apoptosis induction with multiple stimuli, cytochrome c release and caspase activation measurements FEBS letters Medium 11557035
2013 BCL-B promotes lung cancer invasiveness by direct interaction with the effector protein BOK; this interaction promotes sublethal MOMP generating apoptosis-flatliners that become drug-tolerant persister cells, and engages EMT to enhance cancer cell invasiveness. Co-immunoprecipitation, MOMP assays, drug-tolerant persister cell characterization, EMT marker analysis Cells Medium 39996719

Source papers

Stage 0 corpus · 60 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Boo, a novel negative regulator of cell death, interacts with Apaf-1. The EMBO journal 143 9878060
2008 Differential regulation of Bax and Bak by anti-apoptotic Bcl-2 family proteins Bcl-B and Mcl-1. The Journal of biological chemistry 114 18178565
2001 Bcl-B, a novel Bcl-2 family member that differentially binds and regulates Bax and Bak. The Journal of biological chemistry 104 11278245
2012 Bcl-2 is a better ABT-737 target than Bcl-xL or Bcl-w and only Noxa overcomes resistance mediated by Mcl-1, Bfl-1, or Bcl-B. Cell death & disease 74 22875003
2012 BCL2L10 is a predictive factor for resistance to azacitidine in MDS and AML patients. Oncotarget 71 22577154
2007 Nur77 converts phenotype of Bcl-B, an antiapoptotic protein expressed in plasma cells and myeloma. Blood 71 17227826
2016 IRBIT controls apoptosis by interacting with the Bcl-2 homolog, Bcl2l10, and by promoting ER-mitochondria contact. eLife 62 27995898
2012 Ubiquitination, localization, and stability of an anti-apoptotic BCL2-like protein, BCL2L10/BCLb, are regulated by Ubiquilin1. Proceedings of the National Academy of Sciences of the United States of America 62 22233804
2012 The restricted binding repertoire of Bcl-B leaves Bim as the universal BH3-only prosurvival Bcl-2 protein antagonist. Cell death & disease 61 23235460
2001 Bcl2-L-10, a novel anti-apoptotic member of the Bcl-2 family, blocks apoptosis in the mitochondria death pathway but not in the death receptor pathway. Human molecular genetics 59 11689480
2019 The role of the apoptosis-related protein BCL-B in the regulation of mitophagy in hepatic stellate cells during the regression of liver fibrosis. Experimental & molecular medicine 51 30635551
2008 Bcl-B expression in human epithelial and nonepithelial malignancies. Clinical cancer research : an official journal of the American Association for Cancer Research 50 18483366
2012 The anti-apoptotic Bcl-B protein inhibits BECN1-dependent autophagic cell death. Autophagy 44 22498477
2009 Oocytes and early embryos selectively express the survival factor BCL2L10. Journal of molecular medicine (Berlin, Germany) 37 19551325
2018 Breast Cancer Targeting through Inhibition of the Endoplasmic Reticulum-Based Apoptosis Regulator Nrh/BCL2L10. Cancer research 36 29330143
2007 NM23-H2 involves in negative regulation of Diva and Bcl2L10 in apoptosis signaling. Biochemical and biophysical research communications 35 17532299
2010 BCL2L10 protein regulates apoptosis/proliferation through differential pathways in gastric cancer cells. The Journal of pathology 34 21171085
2001 Characterization of NR13-related human cell death regulator, Boo/Diva, in normal and cancer tissues. Biochimica et biophysica acta 32 11566354
2003 Characterization of the anti-apoptotic mechanism of Bcl-B. The Biochemical journal 31 12921534
2009 Role of Bcl2-like 10 (Bcl2l10) in Regulating Mouse Oocyte Maturation. Biology of reproduction 30 19439730
2010 Homology modeling and docking studies of human Bcl-2L10 protein. Journal of biomolecular structure & dynamics 27 20919753
2021 The roles of MCP-1/CCR2 mediated macrophage recruitment and polarization in bladder outlet obstruction (BOO) induced bladder remodeling. International immunopharmacology 24 34311189
2016 BCL-B (BCL2L10) is overexpressed in patients suffering from multiple myeloma (MM) and drives an MM-like disease in transgenic mice. The Journal of experimental medicine 23 27455953
2010 BCL2L10 is frequently silenced by promoter hypermethylation in gastric cancer. Oncology reports 22 20428828
2009 HIP1R interacts with a member of Bcl-2 family, BCL2L10, and induces BAK-dependent cell death. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 22 19255499
2013 The BCL2L10 Leu21Arg variant and risk of therapy-related myeloid neoplasms and de novo myelodysplastic syndromes. Leukemia & lymphoma 21 24047476
2020 BCL2L10 Is Overexpressed in Melanoma Downstream of STAT3 and Promotes Cisplatin and ABT-737 Resistance. Cancers 19 33396645
2018 MicroRNA-18a promotes hepatocellular carcinoma proliferation, migration, and invasion by targeting Bcl2L10. OncoTargets and therapy 18 30519035
2016 BCL2L10 inhibits growth and metastasis of hepatocellular carcinoma both in vitro and in vivo. Molecular carcinogenesis 18 27770580
2018 Boo-boos as the building blocks of pain expression: An observational examination of parental responses to everyday pain in toddlers. Canadian journal of pain = Revue canadienne de la douleur 17 35005368
2019 BCL2L10/BECN1 modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway. Aging 16 30696802
2013 Polyubiquitination and proteasomal turnover controls the anti-apoptotic activity of Bcl-B. Oncogene 16 23563182
2001 Diva/Boo is a negative regulator of cell death in human glioma cells. FEBS letters 16 11557035
2018 MicroRNA-101 protects bladder of BOO from hypoxia-induced fibrosis by attenuating TGF-β-smad2/3 signaling. IUBMB life 14 30549198
2023 Bcl-B: an "unknown" protein of the Bcl-2 family. Biology direct 13 37899453
2011 Characterization of unique signature sequences in the divergent maternal protein Bcl2l10. Molecular biology and evolution 11 21705382
2021 UBQLN4 is an ATM substrate that stabilizes the anti-apoptotic proteins BCL2A1 and BCL2L10 in mesothelioma. Molecular oncology 10 34245648
2008 A TR3/Nur77 peptide-based high-throughput fluorescence polarization screen for small molecule Bcl-B inhibitors. Journal of biomolecular screening 10 18626112
2021 BOO induces fibrosis and EMT in urothelial cells which can be recapitulated in vitro through elevated storage and voiding pressure cycles. International urology and nephrology 9 34232473
2020 Urethral meatus stricture BOO stimulates bladder smooth muscle cell proliferation and pyroptosis via IL‑1β and the SGK1‑NFAT2 signaling pathway. Molecular medicine reports 9 32468047
2019 Bcl2l10 mediates the proliferation, invasion and migration of ovarian cancer cells. International journal of oncology 9 31894274
2020 Severe Phenotype in a Patient With Homozygous 15q21.2 Microdeletion Involving BCL2L10, GNB5, and MYO5C Genes, Resembling Infantile Developmental Disorder With Cardiac Arrhythmias (IDDCA). Frontiers in genetics 8 32477400
2013 Subcellular dynamics of the maternal cell death regulator BCL2L10 in human preimplantation embryos. Human reproduction (Oxford, England) 8 23293224
2021 Bcl2l10 induces metabolic alterations in ovarian cancer cells by regulating the TCA cycle enzymes SDHD and IDH1. Oncology reports 7 33649794
2016 Bcl2l10, a new Tpx2 binding partner, is a master regulator of Aurora kinase A in mouse oocytes. Cell cycle (Georgetown, Tex.) 6 27753540
2017 Role of BCL2L10 in regulating buffalo (Bubalus bubalis) oocyte maturation. Theriogenology 5 29331495
2004 Effect of Boo Yong-Tang on mast cell-mediated allergic reaction. Immunopharmacology and immunotoxicology 5 15518177
2012 Nuclear magnetic resonance study of protein-protein interactions involving apoptosis regulator Diva (Boo) and the BH3 domain of proapoptotic Bcl-2 members. Journal of molecular recognition : JMR 4 23192964
2023 Molecular dynamics simulations assisted investigation of phytochemicals as potential lead candidates against anti-apoptotic Bcl-B protein. Journal of biomolecular structure & dynamics 3 38111145
2022 Expression patterns and biological function of BCL2L10 during mouse preimplantation development. Gene expression patterns : GEP 3 36341977
2021 circTADA2A Retards the Progression of Colorectal Cancer via Regulating miR-1229/BCL2L10 Signal Axis. Cancer management and research 2 34512021
2017 Asymptomatic bacteriuria in pregnant women attending Boo-Ali Hospital Tehran Iran: Urine analysis vs. urine culture. Electronic physician 2 29403616
2010 Sequence-specific 1H, 13C, and 15N resonance assignments of Diva (Boo), an apoptosis regulator of the Bcl-2 family. Biomolecular NMR assignments 2 20127209
2025 Withania somnifera-derived phytochemicals as Bcl-B inhibitors in cancer therapy: A computational approach from byte to bench to bedside. Biochemical and biophysical research communications 1 39884007
2025 BCL-B Promotes Lung Cancer Invasiveness by Direct Inhibition of BOK. Cells 1 39996719
2025 HuangE Capsules Improve Bladder Function in BOO-induced Overactive Bladder Rats: Network Pharmacology and Experimental Validation. Combinatorial chemistry & high throughput screening 1 40296623
2022 Survivin knockdown alleviates pathological hydrostatic pressure-induced bladder smooth muscle cell dysfunction and BOO-induced bladder remodeling via autophagy. Frontiers in cell and developmental biology 1 36393846
2026 Urothelial Piezo1 channel contributes to BOO-induced inflammation, EMT, and bladder fibrosis via activation of NLRP3 inflammasome. Journal of translational medicine 0 41559677
2025 Pectin Peek-a-Boo: Homogalacturonan Turnover During Flooding-Induced Legume Root Aerenchyma Formation. Plants (Basel, Switzerland) 0 40941785
2023 Retraction: Survivin knockdown alleviates pathological hydrostatic pressure-induced bladder smooth muscle cell dysfunction and BOO-induced bladder remodeling via autophagy. Frontiers in cell and developmental biology 0 37664460

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