Affinage

BCL10

B-cell lymphoma/leukemia 10 · UniProt O95999

Length
233 aa
Mass
26.3 kDa
Annotated
2026-06-09
100 papers in source corpus 49 papers cited in narrative 44 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

BCL10 is a CARD-domain adaptor protein that serves as the central signal-amplifying scaffold linking antigen and G protein-coupled receptors to canonical NF-κB activation (PMID:11163238, PMID:17101977). Its N-terminal CARD mediates homo-oligomerization, an activity essential for both NF-κB activation and, in overexpression settings, caspase-9-dependent apoptosis (PMID:9989495, PMID:10319863, PMID:10187815, PMID:10187770, PMID:10364242). Upon receptor engagement, CARMA/CARD scaffolds (CARMA1 in lymphocytes, CARMA3 in non-immune cells, CARD9 in myeloid contexts) bind the BCL10 CARD and nucleate cooperative, unidirectional BCL10 CARD filament assembly, which recruits BCL10 to membrane lipid rafts at the immunological synapse and templates MALT1 dimerization and TRAF6 decoration into a higher-order CBM signalosome (PMID:11356195, PMID:11278692, PMID:11053425, PMID:14673152, PMID:24074955, PMID:29382759). Within this assembly BCL10 oligomers, together with MALT1 paracaspase activity, drive TRAF6/UBC13- and LUBAC/HOIP-dependent K63-linked and linear (M1) polyubiquitination of BCL10 itself (at K17/K31/K63) and of NEMO/IKKγ, recruiting and activating the IKK complex via TAK1 to trigger IκBα degradation and NF-κB nuclear translocation (PMID:14695475, PMID:15125833, PMID:18287044, PMID:27777308). BCL10 signaling is selective for the NF-κB branch, being dispensable for Ca2+ flux, MAPK/AP-1, and mTOR activation downstream of these receptors (PMID:11163238, PMID:17095601, PMID:24917592). Signal output is tightly bounded by a phosphorylation and degradation network: CaMKII (Ser138), RIP2, IKKβ, and Akt1 phosphorylate BCL10 with both activating and feedback-terminating consequences, calcineurin dephosphorylates BCL10 to sustain CBM assembly, and BCL10 is degraded through NEDD4/Itch- and cIAP2-driven lysosomal, p62-dependent autophagic, and β-TrCP-dependent proteasomal routes (PMID:15082780, PMID:16818229, PMID:16395405, PMID:17052756, PMID:21513986, PMID:17371994, PMID:17502353, PMID:17213322, PMID:21199863, PMID:22658522). BCL10 also performs an NF-κB-independent function in actin and membrane remodeling, controlling Fcγ/TCR-induced actin polymerization and phagocytic cup closure through a complex with the clathrin adaptors AP1/EpsinR that delivers the OCRL phosphatase to the phagocytic cup (PMID:17371994, PMID:23153494). Activating CARD missense and C-terminal truncating BCL10 mutations drive constitutive CBM signaling in ABC-DLBCL and confer distinct therapeutic vulnerabilities (PMID:35658124).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1999 High

    Established the founding molecular activity of BCL10: that its N-terminal CARD drives self-oligomerization, which is required both to activate NF-κB and to engage caspase-9-dependent apoptosis, defining BCL10 as a bifunctional CARD adaptor.

    Evidence Overexpression, mutational analysis, NF-κB reporter and caspase processing assays in 293/MCF-7 cells

    PMID:10187770 PMID:10187815 PMID:10319863 PMID:10364242 PMID:9989495

    Open questions at the time
    • Performed in overexpression systems; physiological relevance of the apoptotic arm not established
    • Did not identify upstream receptors or scaffolds engaging BCL10
  2. 1999 High

    Placed BCL10 in the NF-κB cascade upstream of IKKα via a NIK-dependent route, showing the CARD is both necessary and sufficient for signaling.

    Evidence Dominant-negative NIK/IκBα constructs and NF-κB reporter assays

    PMID:10187770 PMID:10364242

    Open questions at the time
    • Did not define the receptor input or direct downstream ubiquitination targets
    • NIK-dependence later refined to canonical IKK activation
  3. 2001 High

    Genetic knockout demonstrated that BCL10 is specifically required for antigen-receptor-induced NF-κB in lymphocytes while sparing Ca2+, MAPK, and AP-1 signaling, fixing BCL10 to the NF-κB branch in vivo.

    Evidence Bcl10-deficient mice with lymphocyte stimulation and pathway-specific NF-κB assays

    PMID:11163238

    Open questions at the time
    • Did not resolve the molecular bridge between the receptor and BCL10
    • Mechanism of NF-κB-branch selectivity unexplained
  4. 2001 High

    Defined the core CBM assembly by showing BCL10 bridges CARMA-type scaffolds to MALT1, oligomerizing and activating the MALT1 caspase-like domain for synergistic IKK-dependent NF-κB activation.

    Evidence Co-immunoprecipitation, ternary complex reconstitution, dominant-negative NF-κB reporter assays; CARMA1/CARD11 CARD-CARD binding and BCL10 translocation imaging

    PMID:11262391 PMID:11278692 PMID:11356195 PMID:11387339

    Open questions at the time
    • Did not show how MALT1 oligomerization leads to IKK activation biochemically
    • Structural basis of CARD-CARD nucleation unknown
  5. 2003 High

    Identified the biochemical output of the CBM complex: BCL10/MALT1 direct K63-linked polyubiquitination of NEMO/IKKγ via UBC13, defining ubiquitin signaling as the link to IKK activation.

    Evidence siRNA knockdown, in vitro ubiquitination, NEMO ubiquitination-site mutants, NF-κB reporter assays; RIP2 association/phosphorylation of BCL10 from knockout mice

    PMID:14638696 PMID:14695475

    Open questions at the time
    • E3 ligase responsible not yet pinned to TRAF6
    • Order of BCL10 vs NEMO ubiquitination unresolved
  6. 2004 High

    Reconstituted the activation mechanism with purified components, showing oligomeric BCL10/MALT1 binds and activates TRAF6 ligase, which polyubiquitinates NEMO and engages TAK1 to activate IKK, and localized assembly to immunological-synapse lipid rafts.

    Evidence In vitro reconstitution with purified proteins, gel filtration of oligomers, RNAi; lipid raft fractionation and CARMA1-deficient T cell complementation

    PMID:14673152 PMID:15125833

    Open questions at the time
    • Did not visualize the higher-order architecture of the active complex
    • How oligomerization threshold is set in cells unknown
  7. 2004 Medium

    Revealed signal termination logic by showing TCR-induced lysosomal degradation of BCL10 driven by HECT E3 ligases NEDD4/Itch, selectively shutting down NF-κB.

    Evidence Proteasome inhibitors, lysosome fractionation, E3 ligase overexpression/knockdown, NF-κB assays

    PMID:15082780

    Open questions at the time
    • Single lab; relative contribution of lysosomal vs other degradation routes unquantified
    • Ubiquitin linkage type targeting BCL10 to lysosome not defined
  8. 2004 Medium

    Extended BCL10 function beyond antigen receptors to innate TLR4 signaling, showing recruitment to TLR4 complexes and a requirement for LPS-induced NF-κB, with SOCS3 as a negative regulator.

    Evidence Co-IP, BCL10-deficient macrophage line, SOCS3 overexpression, NF-κB reporter assays; IRAK-1/Pellino2 interactions and fractionation

    PMID:15213237 PMID:16831874

    Open questions at the time
    • TLR4-to-BCL10 connection less defined than antigen-receptor axis
    • Single-lab Co-IP and fractionation without reconstitution
  9. 2005 Medium

    Uncovered nucleocytoplasmic regulation of BCL10: MALT1 NES-driven export controls BCL10 cytoplasmic localization, while Akt1 phosphorylation (Ser218/Ser231) and Bcl3 binding drive TNFα-induced BCL10 nuclear entry, with NF-κB autoregulating BCL10 transcription.

    Evidence MALT1 NES mutagenesis and leptomycin B; Akt1 kinase assay, Bcl3 Co-IP, ChIP/EMSA, inhibitor validation

    PMID:16123224 PMID:16280327

    Open questions at the time
    • Functional role of nuclear BCL10 not fully defined
    • Single-lab studies for each localization branch
  10. 2006 High

    Generalized BCL10 to GPCR signaling via CARMA3-BCL10-MALT1 signalosomes (angiotensin II, LPA) and to multiple immune effector contexts (mast cells, NK cells), each selectively controlling the NF-κB/cytokine arm while sparing other outputs.

    Evidence Bcl10-/- mice and MEFs, dominant-negative/RNAi, IKKγ ubiquitination and cytokine assays, parallel pathway dissection in mast and NK cells

    PMID:16432253 PMID:17095601 PMID:17101977 PMID:18192506

    Open questions at the time
    • Tissue-specific scaffold partners for each receptor not all mapped
    • Mechanism of NF-κB-branch selectivity remained unexplained
  11. 2006 High

    Defined a multi-kinase phosphoregulatory network on BCL10 — CaMKII (Ser138) priming ubiquitination, IKKβ and the IKK complex driving negative-feedback disassembly and β-TrCP/proteasomal degradation — quantitatively tuning NF-κB output.

    Evidence In vitro kinase assays, phospho-site mutagenesis (S138A, IKK sites), ubiquitination/degradation and IL-2 assays in primary T cells

    PMID:16818229 PMID:17052756 PMID:17213322 PMID:17371994 PMID:17502353 PMID:21513986

    Open questions at the time
    • Temporal coordination of competing kinases not fully resolved
    • Some phospho-site assignments from single labs
  12. 2006 Medium

    Showed BCL10 also scaffolds JNK2 signaling and identified cIAP2 as an E3 ligase degrading BCL10, with loss of this activity in the cIAP2-MALT1 lymphoma fusion stabilizing BCL10.

    Evidence Endogenous Co-IP and JNK isoform-specific kinase assays; in vitro ubiquitination, stability and cytokine assays

    PMID:16395405 PMID:17189706

    Open questions at the time
    • JNK2 scaffolding role from single lab
    • Physiological substrate scope of cIAP2 toward BCL10 not generalized
  13. 2007 Medium

    Separated BCL10's NF-κB function from a distinct, phosphorylation-dependent role in actin polymerization and phagocytosis, showing S138A selectively blocks actin remodeling without affecting NF-κB.

    Evidence BCL10 siRNA, S138A mutagenesis, F-actin staining, phagocytosis and NF-κB reporter assays

    PMID:17371994

    Open questions at the time
    • Effector machinery linking BCL10 to actin not yet identified
    • Single-lab knockdown study
  14. 2008 High

    Resolved the ubiquitin code on BCL10 by showing K63-linked ubiquitination at K31/K63 specifically mediates NEMO recruitment downstream of CBM assembly, separating complex formation from IKK recruitment; refined the BCL10 CARD-MALT1 interaction interfaces; and mapped CARD11 cofactor recruitment.

    Evidence Linkage-specific ubiquitin assays, lysine mutagenesis, NEMO-binding assays; FRET, Co-IP, point mutagenesis and modeling; RNAi rescue in deficient cells

    PMID:18287044 PMID:18625728 PMID:18806265

    Open questions at the time
    • E3 ligase placing these chains on BCL10 not definitively assigned
    • Interaction-mapping studies single-lab
  15. 2011 Medium

    Established positive-feedback dephosphorylation by calcineurin sustaining CBM assembly, and identified MIB2 as an additional BCL10-interacting E3 promoting NEMO ubiquitination and TAK1 activation.

    Evidence In vitro phosphatase assay, calcineurin RNAi and CsA/FK506; proteomic identification, pulldown, knockdown NF-κB assays

    PMID:21199863 PMID:21896478

    Open questions at the time
    • Both single-lab; integration with the IKKβ/β-TrCP negative arms not modeled
    • Substrate residues dephosphorylated by calcineurin not mapped
  16. 2012 Medium

    Mechanistically defined the NF-κB-independent membrane-remodeling role, showing BCL10 partners with AP1/EpsinV clathrin adaptors to deliver OCRL phosphatase and drive Rac1/PI3K-dependent phagocytic cup closure; and revealed selective autophagy as a degradation/signaling node requiring K63-ubiquitin and p62.

    Evidence siRNA depletion, phagocytosis/Rac1/PI3K assays, AP1/EpsinR Co-IP, PI(4,5)P2 imaging; autophagy inhibition, p62 knockout, BCL10 degradation/NF-κB assays

    PMID:22658522 PMID:23153494

    Open questions at the time
    • AP1/EpsinR-OCRL pathway from single lab
    • How phosphorylation gates the choice between NF-κB and actin functions unresolved
  17. 2013 High

    Provided the structural mechanism: CARMA1 nucleates cooperative, threshold-sensitive, unidirectional BCL10 CARD filament formation that templates MALT1 dimerization/activation and TRAF6 decoration into higher-order CBM assemblies.

    Evidence Cryo-EM, crystallography, NMR, in vitro filament reconstitution, structure-guided mutagenesis with NF-κB readouts; live-cell time-lapse imaging of polymerization

    PMID:24074955 PMID:29382759

    Open questions at the time
    • How ubiquitination machinery docks onto the filament structurally not resolved
    • In vivo filament dynamics in primary cells not quantified
  18. 2014 Medium

    Defined effector-T-cell-specific signalosome wiring (p62-BCL10-MALT1-IKK clustering) and sharpened the functional boundary of BCL10 by showing it is dispensable for CARMA1/MALT1-dependent mTOR activation.

    Evidence Co-IP, p62-deficient T cells, confocal imaging, IKK assays; BCL10-deficient T cell mTOR/metabolic assays

    PMID:24825920 PMID:24917592

    Open questions at the time
    • Both single-lab
    • Molecular basis distinguishing BCL10-dependent NF-κB from BCL10-independent mTOR branch unresolved
  19. 2016 High

    Identified linear (M1) ubiquitination of BCL10 at K17/K31/K63 by LUBAC/HOIP, co-recruited with substrate by CARD11, as a required step for NEMO/IKK recruitment, adding a second ubiquitin chain type to BCL10 signaling.

    Evidence Linkage-specific ubiquitin assays, lysine mutagenesis, HOIP/LUBAC knockdown, CARD11 Co-IP, NF-κB reporter assays

    PMID:27777308

    Open questions at the time
    • Interplay between K63 and M1 chains on the same lysines not deconvolved
    • Single-lab study
  20. 2018 Medium

    Added GSK3β as an upstream kinase whose site-specific phosphorylation of BCL10 promotes CBM assembly and downstream MALT1 protease activity.

    Evidence GSK3β inhibitors and RNAi, BCL10 phosphorylation and MALT1 substrate-cleavage assays

    PMID:29358699

    Open questions at the time
    • Phosphorylation sites not precisely mapped
    • Single-lab, largely pharmacological
  21. 2019 High

    Established the physiological importance of CBM/MALT1 protease activity for regulatory T cell suppressive function, showing acute BCL10 loss in mature Tregs causes lethal autoimmunity.

    Evidence Conditional Bcl10 knockout in Tregs, suppression and colitis-transfer assays, MALT1 inhibitor validation

    PMID:31138793

    Open questions at the time
    • BCL10-dependent transcriptional targets governing suppression not fully mapped
    • Does not address BCL10 in conventional T cell tolerance
  22. 2022 High

    Connected BCL10 biology to disease by defining two biochemically distinct oncogenic BCL10 mutation classes in ABC-DLBCL — filament-stabilizing CARD missense and MALT1-disinhibiting C-terminal truncations — with divergent BTK- and MALT1-inhibitor sensitivities.

    Evidence Structural analysis, polymerization and MALT1 activity assays, drug-sensitivity testing in primary lymphoma and cell lines

    PMID:35658124

    Open questions at the time
    • Frequency and prognostic impact across patient cohorts not addressed here
    • Resistance mechanisms beyond these two classes unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple competing phosphorylation, ubiquitination, dephosphorylation, and degradation inputs are temporally integrated on the BCL10 filament to set NF-κB amplitude and duration, and what structurally distinguishes BCL10's NF-κB scaffolding from its actin/membrane-remodeling function, remain open.
  • No unified quantitative model coupling filament dynamics to PTM cycles
  • Structural basis of the NF-κB-independent AP1/EpsinR/OCRL function undetermined
  • Direct E3 ligases for each BCL10 ubiquitin chain type not all assigned

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0140096 catalytic activity, acting on a protein 3
Localization
GO:0005829 cytosol 3 GO:0005634 nucleus 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 1 R-HSA-5653656 Vesicle-mediated transport 1
Partners
AKT1CARD11CARD9IKBKGMALT1RIPK2SQSTM1TRAF6
Complex memberships
BCL10-AP1/EpsinR complexCBM signalosome (CARMA1/CARD11-BCL10-MALT1)p62-BCL10-MALT1-IKK signalosome

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 BCL10 contains an N-terminal CARD domain that mediates homodimerization/oligomerization; CARD-mediated oligomerization is essential for both NF-κB activation and apoptosis induction. Wild-type BCL10 activates NF-κB and induces apoptosis, while C-terminal truncation mutants retain NF-κB activation but lose pro-apoptotic activity. Overexpression in 293/MCF7 cells, mutational analysis, NF-κB reporter assays, apoptosis assays Cell High 10319863 9989495
1999 BCL10 (also called mE10/CIPER/CLAP/c-E10) contains an N-terminal CARD that forms homodimers; the C-terminal region binds pro-caspase-9 and promotes its autoproteolytic activation to induce apoptosis, with CARD-mediated oligomerization being essential for killing activity. Overexpression in MCF-7 cells, co-immunoprecipitation, mutational analysis, caspase processing assay The Journal of biological chemistry High 10187770 10187815 10364242
1999 BCL10 CARD domain activates NF-κB through a NIK-dependent pathway upstream of IKKα; the CARD is both necessary and sufficient for NF-κB activation and for homodimerization. Mutational analysis, dominant-negative NIK/IκBα constructs, NF-κB reporter assays The Journal of biological chemistry High 10187770 10364242
2001 BCL10 is a positive regulator of antigen receptor-induced NF-κB activation in B and T lymphocytes. BCL10-deficient mice show complete absence of antigen receptor-induced NF-κB activation while retaining normal Ca2+ signaling, MAPK, and AP-1 activation, placing BCL10 specifically in the NF-κB branch downstream of antigen receptors. Bcl10 knockout mice, lymphocyte stimulation assays, NF-κB activation assays, genetic epistasis Cell High 11163238
2001 BCL10 and MALT1 form a specific protein complex; BCL10 mediates oligomerization and activation of the MALT1 caspase-like domain, and together they synergistically activate NF-κB through the IKK complex. BCL10 bridges the BIMP1/MALT1 interaction in a ternary complex. Co-immunoprecipitation, NF-κB reporter assays, dominant-negative mutant analysis The Journal of biological chemistry High 11262391 11387339
2001 CARD11/CARMA1 binds BCL10 via CARD-CARD interaction, induces phosphorylation of BCL10, and translocates BCL10 from cytoplasm to perinuclear structures, thereby activating NF-κB. CARD11 and CARD14 both associate specifically with the BCL10 CARD domain. Co-immunoprecipitation, co-transfection, subcellular localization by immunofluorescence, NF-κB reporter assays FEBS letters / The Journal of biological chemistry High 11278692 11356195
2000 CARD9 directly interacts with the BCL10 CARD domain (but not other CARD-containing proteins), forms a pre-existing signaling complex with endogenous BCL10, and activates NF-κB as an upstream activator of BCL10. Mammalian two-hybrid, co-immunoprecipitation of endogenous proteins, NF-κB reporter assays The Journal of biological chemistry Medium 11053425
2003 BCL10 activates NF-κB by targeting NEMO/IKKγ for K63-linked polyubiquitination, requiring MALT1 (paracaspase) and UBC13 as a ubiquitin-conjugating enzyme. A NEMO mutant unable to be ubiquitinated blocks BCL10-induced NF-κB activation. siRNA knockdown, ubiquitination assays, NEMO ubiquitination-site mutants, NF-κB reporter assays Nature High 14695475
2004 TRAF6 ubiquitin ligase and TAK1 kinase mediate IKK activation downstream of BCL10 and MALT1. Only oligomeric (high-molecular-weight) forms of BCL10 and MALT1 can activate IKK in vitro. MALT1 oligomers bind TRAF6, induce TRAF6 oligomerization, and activate TRAF6 ligase activity to polyubiquitinate NEMO. In vitro reconstitution with purified proteins, RNAi silencing, IKK activation assays, gel filtration to isolate oligomers Molecular cell High 15125833
2004 CARMA1 recruits BCL10 and IKKβ into lipid rafts of the immunological synapse in a CD3/CD28-dependent manner; CARMA1 membrane association is required for this recruitment, and a CARMA1 mutant unable to associate with BCL10 fails to rescue NF-κB activation. Lipid raft fractionation, immunological synapse imaging, CARMA1-deficient T cell complementation assays Molecular and cellular biology High 14673152
2004 BCL10 degradation following TCR/PKC stimulation occurs via the lysosomal pathway (not proteasome), requires an intact CARD domain, and is promoted by HECT-domain ubiquitin ligases NEDD4 and Itch, which ubiquitinate BCL10. This degradation selectively terminates IKK/NF-κB signaling. Proteasome inhibitor treatment, lysosome fractionation, ubiquitin ligase overexpression/knockdown, NF-κB activity assays Molecular and cellular biology Medium 15082780
2006 IKKβ plays a dual role at the CBM complex: it is required for initial CBM complex formation, but upon engagement IKKβ phosphorylates BCL10 at its C-terminus, disrupting BCL10/MALT1 association and BCL10-mediated IKKγ ubiquitination, thereby providing negative feedback. Mutation of IKKβ phosphorylation sites on BCL10 enhances NF-κB target gene expression. Co-immunoprecipitation, IKKβ phosphorylation site mutagenesis, primary T cell NF-κB reporter assays, IL-2/TNFα measurement Molecular cell High 16818229
2006 cIAP2 functions as an E3 ubiquitin ligase for BCL10, targeting it for degradation and thereby inhibiting antigen receptor-mediated cytokine production. The cIAP2-MALT1 fusion protein lacks E3 activity, leading to BCL10 stabilization in MALT lymphomas. In vitro ubiquitination assay, co-immunoprecipitation, BCL10 protein stability assays, cytokine production assays The Journal of clinical investigation High 16395405
2006 BCL10 and MALT1 are essential for FcεRI-mediated NF-κB activation and pro-inflammatory cytokine production in mast cells, but are dispensable for degranulation and leukotriene secretion, demonstrating that BCL10 selectively controls the NF-κB arm downstream of FcεRI. Bcl10−/− and Malt1−/− mice, mast cell stimulation, cytokine ELISA, degranulation assays The Journal of experimental medicine High 16432253
2006 CARMA3/BCL10/MALT1 form a signalosome that mediates angiotensin II receptor (GPCR)-dependent NF-κB activation in hepatocytes and vascular cells, acting through IKKγ ubiquitination. BCL10-deficient mice show defective hepatic cytokine production after Ang II treatment. Dominant-negative mutants, RNAi, gene targeting (Bcl10−/− mice), IKKγ ubiquitination assay, cytokine ELISA Proceedings of the National Academy of Sciences of the United States of America High 17101977
2006 BCL10 and MALT1 are required for lysophosphatidic acid (LPA)-induced NF-κB activation and IL-6 production downstream of G protein-coupled receptors in non-immune cells, cooperating with PKC. BCL10/MALT1 are dispensable for LPA-activated JNK, p38, ERK, and Akt. Bcl10−/− and Malt1−/− mouse embryonic fibroblasts, IκBα degradation assays, IL-6 ELISA, kinase pathway analysis Proceedings of the National Academy of Sciences of the United States of America High 17095601
2007 BCL10 is phosphorylated at Ser138 by CaMKII following TCR stimulation; phosphorylation at this residue by CaMKII is required for CaMKII's ability to regulate interactions within the Carma1-BCL10-MALT1 complex and for signal-induced ubiquitinations of BCL10 and IKKγ. In vitro kinase assay (CaMKII + BCL10), CaMKII inhibitor KN93, CaMKII siRNA, S138A mutagenesis, NF-κB reporter assays Molecular immunology High 17052756 21513986
2006 Phosphorylation of BCL10 at Ser138 negatively regulates NF-κB activation: the S138A mutation impairs TCR-induced ubiquitination and subsequent degradation of BCL10, prolonging NF-κB activation and enhancing IL-2 production. Phosphorylation site mutagenesis (S138A), ubiquitination assays, NF-κB reporter assays, IL-2 ELISA Journal of immunology / Molecular and cellular biology High 17371994 17502353
2007 IKK complex phosphorylates BCL10 after TCR stimulation and causes its proteolysis via the β-TrCP ubiquitin ligase/proteasome pathway, providing a negative feedback loop. BCL10 mutants at IKK phosphorylation sites are resistant to degradation, accumulate in the nucleus, and increase IL-2 production. In vitro IKK kinase assay, proteasome inhibitors, β-TrCP overexpression, phosphorylation-site mutagenesis, IL-2 measurement Proceedings of the National Academy of Sciences of the United States of America High 17213322
2007 BCL10 (but not CARMA1) controls TCR-induced and FcγR-induced actin polymerization independently of NF-κB activation. Phosphorylation-deficient S138A BCL10 specifically inhibits TCR-induced actin polymerization without affecting NF-κB. BCL10 silencing impairs phagocytosis in monocytes. BCL10 siRNA, S138A mutagenesis, F-actin staining, phagocytosis assays, NF-κB reporter assays Journal of immunology Medium 17371994
2008 K63-linked polyubiquitination of BCL10 at residues K31 and K63 is required for NEMO/IKKγ binding and NF-κB activation following TCR stimulation. Mutation of these ubiquitination sites prevents NEMO recruitment without affecting CBM complex assembly. K63-ubiquitin linkage-specific assays, BCL10 ubiquitination site mutagenesis (K31R, K63R), NEMO binding assay, NF-κB reporter assays Proceedings of the National Academy of Sciences of the United States of America High 18287044
2008 Bcl10-MALT1 interaction involves multiple protein domains: a 13-aa region C-terminal to the Bcl10 CARD interacts with MALT1 Ig-like domains, and additionally the MALT1 death domain and BCL10 CARD (especially residues D80 and E84 of helix 5) contribute to the interaction. CARD mutations that disrupt folding strongly impair BCL10-MALT1 interaction. Co-immunoprecipitation, FRET in T cells, point mutagenesis of conserved BCL10 CARD residues, molecular modeling The Journal of biological chemistry Medium 18806265
2008 CARD11 recruits multiple signaling cofactors (BCL10, TRAF6, TAK1, IKKγ, caspase-8) through its CARD and coiled-coil domains in a signal-inducible manner; BCL10 and MALT1 are independently recruited to CARD11 and can associate with certain cofactors independently of one another. RNAi rescue assays, co-immunoprecipitation in BCL10- and MALT1-deficient cells, NF-κB reporter assays Molecular and cellular biology Medium 18625728
2003 RIP2 kinase associates with BCL10 following TCR engagement and phosphorylates BCL10. RIP2-deficient T cells show defective BCL10 phosphorylation and NF-κB activation; kinase-dead RIP2 cannot rescue NF-κB activation in Rip2−/− fibroblasts. Co-immunoprecipitation, Rip2−/− mice, kinase-dead mutant complementation, NF-κB assays, BCL10 phosphorylation assay The Journal of biological chemistry Medium 14638696
2004 BCL10 interacts with Pellino2 downstream of TLR4 in response to LPS; BCL10 is recruited to TLR4 signaling complexes, and this recruitment is negatively regulated by SOCS3. BCL10-deficient macrophages show defective LPS-induced NF-κB activation while AP-1 and Elk-1 signaling remain intact. Co-immunoprecipitation, BCL10-deficient macrophage cell line, SOCS3 overexpression, NF-κB reporter assays The Journal of biological chemistry Medium 15213237
2006 BCL10 and MALT1 are required for NK cell-mediated NF-κB and JNK/p38 MAPK activation downstream of ITAM-coupled receptors (NK1.1, Ly49D, Ly49H, NKG2D), and depend on CARMA1 (not CARD9). These cascades selectively control cytokine/chemokine production but not cytotoxicity. Bcl10−/−, Malt1−/−, Carma1−/−, Card9−/− primary NK cells, cytokine production assays, cytotoxicity assays, NF-κB reporter assays Blood High 18192506
2006 CARMA1-BCL10 complex selectively regulates JNK2 (not JNK1) after TCR stimulation: BCL10 is inducibly associated with JNK2 and acts as a JIP-like scaffold to assemble JNK2, MKK7, and TAK1 kinases, regulating c-Jun protein levels. Co-immunoprecipitation, CARMA1/BCL10 knockout cells, JNK isoform-specific analysis, kinase assays Immunity Medium 17189706
2006 BCL10 interacts with IRAK-1 upstream in the TLR4 pathway; upon BCL10 dissociation from IRAK-1, BCL10 translocates to cytosol with TRAF6 and TAK1 via a direct BCL10-Pellino2 interaction. BCL10 oligomerization is a prerequisite for its function in LPS-induced NF-κB signaling. Co-immunoprecipitation, siRNA against MALT1, subcellular fractionation, NF-κB activation assays The Journal of biological chemistry Medium 16831874
2011 Calcineurin (Ca2+-dependent phosphatase) directly dephosphorylates BCL10 in vivo and in vitro and interacts with the CBM complex; calcineurin activity positively regulates CBM complex formation and TCR-induced NF-κB. BCL10 is hyperphosphorylated when calcineurin is inhibited by CsA or FK506. In vitro phosphatase assay (calcineurin + BCL10), calcineurin A siRNA, CsA/FK506 treatment, co-immunoprecipitation The Journal of biological chemistry Medium 21199863
2011 E3 ubiquitin ligase MIB2 directly interacts with BCL10, promotes autoubiquitination and ubiquitination of IKKγ/NEMO, and recruits/activates TAK1 as part of the activated BCL10 complex. MIB2 knockdown inhibits BCL10-dependent NF-κB activation. Proteomic identification, in vitro pulldown, overexpression NF-κB assays, MIB2 knockdown The Journal of biological chemistry Medium 21896478
2012 BCL10 has an NF-κB-independent role in actin and membrane remodeling downstream of FcγR in macrophages. BCL10 depletion impairs Rac1 and PI3K activation and leads to abortive phagocytic cups. BCL10 forms a complex with clathrin adaptors AP1 and EpsinR and is required to deliver the OCRL phosphatase (which regulates PI(4,5)P2 and F-actin) to the phagocytic cup. BCL10 depletion by siRNA, phagocytosis assays, Rac1/PI3K activation assays, co-immunoprecipitation with AP1/EpsinR, PI(4,5)P2 imaging Developmental cell Medium 23153494
2012 TCR engagement triggers selective autophagy of BCL10 in effector (but not naive) T cells, requiring K63-polyubiquitination of BCL10 and subsequent association with the autophagy adaptor p62. p62 binding is required for both BCL10 signaling to NF-κB and gradual BCL10 degradation; blockade of BCL10 autophagy enhances NF-κB activation. Autophagy inhibition, ubiquitin linkage-specific assays, p62 knockout/knockdown, BCL10 degradation assays, NF-κB activation Immunity High 22658522
2013 The reconstituted CBM signalosome forms a helical filamentous assembly: CARMA1 nucleates BCL10 filament formation through CARD-CARD interactions in a cooperative, threshold-sensitive manner; MALT1 binds BCL10 filaments and is activated; structure of the BCL10 CARD filament was determined by crystallography, NMR, and EM. Structure-guided mutagenesis confirmed interfaces required for BCL10 filament assembly and MALT1 activation in vitro and NF-κB activation in cells. Cryo-EM, crystallography, NMR, in vitro reconstitution of CBM filament, structure-guided mutagenesis, NF-κB reporter assays Molecular cell High 24074955
2014 BCL10 polymerizes in a unidirectional manner as shown by time-lapse confocal imaging; cryo-EM structure of the BCL10 CARD filament at 4.0 Å resolution redefines CARD-CARD interfaces. CARMA1 serves as a hub forming star-shaped filamentous BCL10 networks and decreases BCL10 polymerization lag time. MALT1 immediately dimerizes on BCL10 filaments, and TRAF6 cooperatively decorates CBM filaments to form higher-order assemblies. Cryo-EM at 4.0 Å, time-lapse confocal imaging, EM of MALT1 and TRAF6 decoration of filaments Proceedings of the National Academy of Sciences of the United States of America High 29382759
2014 A cytosolic p62-BCL10-MALT1-IKK signalosome forms in effector T cells upon TCR stimulation; the active IKK complex is a component of this signalosome; phosphorylated IκBα and NF-κB are transiently recruited before nuclear NF-κB translocation. p62-dependent clustering is required for NF-κB activation in effector T cells. Co-immunoprecipitation, p62-deficient T cells, confocal imaging of signalosome clusters, IKK activity assays Science signaling Medium 24825920
2014 BCL10 is NOT required for TCR/CD28-induced mTOR activation in T cells; this distinguishes the BCL10 requirement for NF-κB from a CARMA1/MALT1-dependent but BCL10-independent pathway to mTOR signaling. BCL10-deficient T cells, mTOR pathway activation assays, metabolic flux assays Science signaling Medium 24917592
2005 MALT1 contains nuclear export signals (NES) and controls the cytoplasmic localization of BCL10; MALT1 is involved in nuclear export of BCL10, shuttling between nucleus and cytoplasm. Leptomycin B (NES inhibitor) retains MALT1 and BCL10 in the nucleus. Deletion mutagenesis of MALT1 NES, leptomycin B treatment, subcellular fractionation and imaging Blood Medium 16123224
2005 BCL10 undergoes nuclear translocation in response to TNFα: Akt1 phosphorylates BCL10 at Ser218 and Ser231, and phosphorylated BCL10 then complexes with Bcl3 to enter the nucleus. An NF-κB-binding site in the BCL10 5'-UTR drives NF-κB-dependent BCL10 upregulation. Chromatin immunoprecipitation, EMSA, Akt1 kinase assay, Bcl3 co-immunoprecipitation, Akt1 inhibitor, Bcl3 depletion The Journal of biological chemistry Medium 16280327
2010 LPS activates the non-canonical NF-κB pathway (RelB/p52) in colonic epithelial cells through BCL10; phosphorylation of BCL10 Ser138 is required for NIK phosphorylation and subsequent RelB/p52 nuclear translocation. Mutation of Ser138 or Ser218 reduces both canonical and non-canonical NF-κB activation. BCL10 siRNA, BCL10 phosphorylation-site mutagenesis (S138G, S218G), nuclear RelB/p52 assays, phospho-NIK assays Experimental cell research Medium 20466000
2009 COP9 signalosome subunit CSN5 interacts with MALT1 and CARMA1; TCR activation recruits CSN to the CBM complex. The CSN is required for maintaining BCL10 stability in response to T cell activation and for TCR-induced IKK activation. Co-immunoprecipitation, CSN5 siRNA knockdown, BCL10 stability assays, IKK activation assays EMBO reports Medium 19444310
2016 BCL10 undergoes TCR-induced conjugation with linearly-linked (M1) polyubiquitin chains (Lin(Ub)n-BCL10) at lysines K17, K31, and K63; linear ubiquitination requires CARD11, MALT1, and the HOIP subunit of LUBAC. Lin(Ub)n-BCL10 is required for NEMO/IKK recruitment. CARD11 co-recruits BCL10 with HOIP to bring substrate to enzyme. Linkage-specific ubiquitin assays, BCL10 lysine mutagenesis, HOIP/LUBAC knockdown, CARD11 co-IP experiments, NF-κB reporter assays The Journal of biological chemistry High 27777308
2018 GSK3β regulates CBM complex formation through site-specific phosphorylation of BCL10; GSK3β inhibition reduces BCL10 phosphorylation, impairs CBM assembly, and consequently reduces MALT1 protease-dependent cleavage of substrates (BCL10, CYLD, RelB), IκBα degradation, and NF-κB activity. GSK3β pharmacological inhibitors (SB216763, SB415286), GSK3β RNAi, BCL10 phosphorylation assays, MALT1 substrate cleavage assays Scientific reports Medium 29358699
2019 BCL10-MALT1 (CBM) signaling mediates TCR-induced NF-κB activation in regulatory T cells and controls their suppressive function; BCL10-dependent MALT1 protease activity is specifically required for Treg suppressive function. Acute BCL10 deletion in mature Tregs impairs suppression and causes lethal autoimmunity. Conditional BCL10 knockout in Tregs (Bcl10fl/fl Foxp3cre), Treg suppression assays, Rag1−/− colitis transfer, gene expression profiling, MALT1 inhibitor treatment Nature communications High 31138793
2022 BCL10 mutations in ABC-DLBCL fall into two biochemically distinct classes: (1) CARD missense mutations enhance BCL10 filament formation via glutamine network structures that stabilize filaments; (2) C-terminal truncating mutations abrogate a MALT1 inhibitory motif, trapping MALT1 in activated filament-bound state. Both classes confer BTK inhibitor resistance, while truncating (not CARD) mutants are hypersensitive to MALT1 inhibitors. Structural analysis, BCL10 polymerization assays, MALT1 activity assays, BTK inhibitor/MALT1 inhibitor drug sensitivity testing in primary lymphoma and cell lines Cancer discovery High 35658124

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 The TRAF6 ubiquitin ligase and TAK1 kinase mediate IKK activation by BCL10 and MALT1 in T lymphocytes. Molecular cell 587 15125833
1999 Bcl10 is involved in t(1;14)(p22;q32) of MALT B cell lymphoma and mutated in multiple tumor types. Cell 535 9989495
2001 Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure. Cell 440 11163238
2003 Bcl10 activates the NF-kappaB pathway through ubiquitination of NEMO. Nature 435 14695475
2001 Bcl10 and MALT1, independent targets of chromosomal translocation in malt lymphoma, cooperate in a novel NF-kappa B signaling pathway. The Journal of biological chemistry 349 11262391
1999 Inactivating mutations and overexpression of BCL10, a caspase recruitment domain-containing gene, in MALT lymphoma with t(1;14)(p22;q32). Nature genetics 311 10319863
2001 CARD11 and CARD14 are novel caspase recruitment domain (CARD)/membrane-associated guanylate kinase (MAGUK) family members that interact with BCL10 and activate NF-kappa B. The Journal of biological chemistry 296 11278692
2000 CARD9 is a novel caspase recruitment domain-containing protein that interacts with BCL10/CLAP and activates NF-kappa B. The Journal of biological chemistry 202 11053425
2010 Antigen receptor signaling to NF-kappaB via CARMA1, BCL10, and MALT1. Cold Spring Harbor perspectives in biology 193 20685844
2004 CD3/CD28 costimulation-induced NF-kappaB activation is mediated by recruitment of protein kinase C-theta, Bcl10, and IkappaB kinase beta to the immunological synapse through CARMA1. Molecular and cellular biology 179 14673152
2020 Camrelizumab Plus Apatinib in Patients With Advanced Cervical Cancer (CLAP): A Multicenter, Open-Label, Single-Arm, Phase II Trial. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 173 33052760
2012 Selective autophagy of the adaptor protein Bcl10 modulates T cell receptor activation of NF-κB. Immunity 172 22658522
2001 Carma1, a CARD-containing binding partner of Bcl10, induces Bcl10 phosphorylation and NF-kappaB activation. FEBS letters 167 11356195
2001 Bimp1, a MAGUK family member linking protein kinase C activation to Bcl10-mediated NF-kappaB induction. The Journal of biological chemistry 154 11387339
2003 Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells. Nature immunology 151 12910267
2013 Structural architecture of the CARMA1/Bcl10/MALT1 signalosome: nucleation-induced filamentous assembly. Molecular cell 150 24074955
2006 CARMA3/Bcl10/MALT1-dependent NF-kappaB activation mediates angiotensin II-responsive inflammatory signaling in nonimmune cells. Proceedings of the National Academy of Sciences of the United States of America 150 17101977
2000 BCL10 expression in normal and neoplastic lymphoid tissue. Nuclear localization in MALT lymphoma. The American journal of pathology 150 11021819
2008 Toll-like receptor 4 mediates induction of the Bcl10-NFkappaB-interleukin-8 inflammatory pathway by carrageenan in human intestinal epithelial cells. The Journal of biological chemistry 138 18252714
1999 CIPER, a novel NF kappaB-activating protein containing a caspase recruitment domain with homology to Herpesvirus-2 protein E10. The Journal of biological chemistry 132 10187770
2013 In planta expression or delivery of potato aphid Macrosiphum euphorbiae effectors Me10 and Me23 enhances aphid fecundity. Molecular plant-microbe interactions : MPMI 122 23194342
2008 NEMO recognition of ubiquitinated Bcl10 is required for T cell receptor-mediated NF-kappaB activation. Proceedings of the National Academy of Sciences of the United States of America 120 18287044
2004 Degradation of Bcl10 induced by T-cell activation negatively regulates NF-kappa B signaling. Molecular and cellular biology 119 15082780
2014 The CARD11-BCL10-MALT1 (CBM) signalosome complex: Stepping into the limelight of human primary immunodeficiency. The Journal of allergy and clinical immunology 116 25087226
2006 Essential role for IkappaB kinase beta in remodeling Carma1-Bcl10-Malt1 complexes upon T cell activation. Molecular cell 111 16818229
2005 MALT lymphoma with t(14;18)(q32;q21)/IGH-MALT1 is characterized by strong cytoplasmic MALT1 and BCL10 expression. The Journal of pathology 107 15682443
2006 The Bcl10-Malt1 complex segregates Fc epsilon RI-mediated nuclear factor kappa B activation and cytokine production from mast cell degranulation. The Journal of experimental medicine 106 16432253
2014 C-type lectin receptor dectin-3 mediates trehalose 6,6'-dimycolate (TDM)-induced Mincle expression through CARD9/Bcl10/MALT1-dependent nuclear factor (NF)-κB activation. The Journal of biological chemistry 103 25202022
1999 mE10, a novel caspase recruitment domain-containing proapoptotic molecule. The Journal of biological chemistry 102 10187815
2014 T cell receptor-dependent activation of mTOR signaling in T cells is mediated by Carma1 and MALT1, but not Bcl10. Science signaling 97 24917592
1999 CLAP, a novel caspase recruitment domain-containing protein in the tumor necrosis factor receptor pathway, regulates NF-kappaB activation and apoptosis. The Journal of biological chemistry 94 10364242
2004 The roles of CARMA1, Bcl10, and MALT1 in antigen receptor signaling. Seminars in immunology 92 15541657
2008 Multiple ITAM-coupled NK-cell receptors engage the Bcl10/Malt1 complex via Carma1 for NF-kappaB and MAPK activation to selectively control cytokine production. Blood 91 18192506
2006 cIAP2 is a ubiquitin protein ligase for BCL10 and is dysregulated in mucosa-associated lymphoid tissue lymphomas. The Journal of clinical investigation 89 16395405
2018 Assembly mechanism of the CARMA1-BCL10-MALT1-TRAF6 signalosome. Proceedings of the National Academy of Sciences of the United States of America 88 29382759
2006 The CARMA1-Bcl10 signaling complex selectively regulates JNK2 kinase in the T cell receptor-signaling pathway. Immunity 88 17189706
2018 The CBM-opathies-A Rapidly Expanding Spectrum of Human Inborn Errors of Immunity Caused by Mutations in the CARD11-BCL10-MALT1 Complex. Frontiers in immunology 86 30283440
2009 BCL2, BCL6, MYC, MALT 1, and BCL10 rearrangements in nodal diffuse large B-cell lymphomas: a multicenter evaluation of a new set of fluorescent in situ hybridization probes and correlation with clinical outcome. Human pathology 86 19144384
2011 The Ca2+-dependent phosphatase calcineurin controls the formation of the Carma1-Bcl10-Malt1 complex during T cell receptor-induced NF-kappaB activation. The Journal of biological chemistry 85 21199863
2000 BCL10 gene mutation in lymphoma. Blood 85 10845924
2006 Bcl10 and Malt1 control lysophosphatidic acid-induced NF-kappaB activation and cytokine production. Proceedings of the National Academy of Sciences of the United States of America 83 17095601
2006 The IRAK-1-BCL10-MALT1-TRAF6-TAK1 cascade mediates signaling to NF-kappaB from Toll-like receptor 4. The Journal of biological chemistry 82 16831874
2014 Inherited BCL10 deficiency impairs hematopoietic and nonhematopoietic immunity. The Journal of clinical investigation 80 25365219
2003 Rip2 participates in Bcl10 signaling and T-cell receptor-mediated NF-kappaB activation. The Journal of biological chemistry 78 14638696
2019 Bcl10-controlled Malt1 paracaspase activity is key for the immune suppressive function of regulatory T cells. Nature communications 75 31138793
2017 The CARMA3-Bcl10-MALT1 Signalosome Drives NFκB Activation and Promotes Aggressiveness in Angiotensin II Receptor-Positive Breast Cancer. Cancer research 74 29259013
2007 Negative feedback loop in T cell activation through IkappaB kinase-induced phosphorylation and degradation of Bcl10. Proceedings of the National Academy of Sciences of the United States of America 74 17213322
2015 Lymphomagenic CARD11/BCL10/MALT1 signaling drives malignant B-cell proliferation via cooperative NF-κB and JNK activation. Proceedings of the National Academy of Sciences of the United States of America 72 26668357
2010 Thrombin-dependent NF-{kappa}B activation and monocyte/endothelial adhesion are mediated by the CARMA3·Bcl10·MALT1 signalosome. The Journal of biological chemistry 69 21041303
1999 c-E10 is a caspase-recruiting domain-containing protein that interacts with components of death receptors signaling pathway and activates nuclear factor-kappaB. The Journal of biological chemistry 69 10400625
2016 Role of the CARMA1/BCL10/MALT1 complex in lymphoid malignancies. Current opinion in hematology 66 27135977
2012 The NF-κB signaling protein Bcl10 regulates actin dynamics by controlling AP1 and OCRL-bearing vesicles. Developmental cell 66 23153494
2010 The CARMA3-Bcl10-MALT1 signalosome promotes angiotensin II-dependent vascular inflammation and atherogenesis. The Journal of biological chemistry 66 20605784
2016 Lymphocyte signaling and activation by the CARMA1-BCL10-MALT1 signalosome. Biological chemistry 64 27420898
2002 BCL10 mutation does not represent an important pathogenic mechanism in gastric MALT-type lymphoma, and the presence of the API2-MLT fusion is associated with aberrant nuclear BCL10 expression. Blood 61 11830492
2008 The monoclonal anti-BCL10 antibody (clone 331.1) is a sensitive and specific marker of pancreatic acinar cell carcinoma and pancreatic metaplasia. Virchows Archiv : an international journal of pathology 60 19066953
2012 Forkhead transcription factor FOXO3a protein activates nuclear factor κB through B-cell lymphoma/leukemia 10 (BCL10) protein and promotes tumor cell survival in serum deprivation. The Journal of biological chemistry 58 22474286
2008 The protein kinase C-responsive inhibitory domain of CARD11 functions in NF-kappaB activation to regulate the association of multiple signaling cofactors that differentially depend on Bcl10 and MALT1 for association. Molecular and cellular biology 58 18625728
2007 CARD-Bcl10-Malt1 signalosomes: missing link to NF-kappaB. Science's STKE : signal transduction knowledge environment 58 17473310
2005 Nuclear expression of BCL10 or nuclear factor kappa B helps predict Helicobacter pylori-independent status of low-grade gastric mucosa-associated lymphoid tissue lymphomas with or without t(11;18)(q21;q21). Blood 57 15845895
2016 Psoriasis mutations disrupt CARD14 autoinhibition promoting BCL10-MALT1-dependent NF-κB activation. The Biochemical journal 55 27071417
2004 Nuclear expression of BCL10 or nuclear factor kappa B predicts Helicobacter pylori-independent status of early-stage, high-grade gastric mucosa-associated lymphoid tissue lymphomas. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 51 15337797
2016 Molecular Determinants of Scaffold-induced Linear Ubiquitinylation of B Cell Lymphoma/Leukemia 10 (Bcl10) during T Cell Receptor and Oncogenic Caspase Recruitment Domain-containing Protein 11 (CARD11) Signaling. The Journal of biological chemistry 50 27777308
2018 Aphid effector Me10 interacts with tomato TFT7, a 14-3-3 isoform involved in aphid resistance. The New phytologist 46 30357852
2013 BCL10 as a useful marker for pancreatic acinar cell carcinoma, especially using endoscopic ultrasound cytology specimens. Pathology international 46 23530562
2007 Bcl10 controls TCR- and FcgammaR-induced actin polymerization. Journal of immunology (Baltimore, Md. : 1950) 46 17371994
2017 Zinc rescues obesity-induced cardiac hypertrophy via stimulating metallothionein to suppress oxidative stress-activated BCL10/CARD9/p38 MAPK pathway. Journal of cellular and molecular medicine 45 28158919
2006 MALT1 and BCL10 aberrations in MALT lymphomas and their effect on the expression of BCL10 in the tumour cells. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 45 16341151
2018 BCL10 - Bridging CARDs to Immune Activation. Frontiers in immunology 44 30022982
2004 BCL10 mediates lipopolysaccharide/toll-like receptor-4 signaling through interaction with Pellino2. The Journal of biological chemistry 43 15213237
2007 Bcl10 mediates LPS-induced activation of NF-kappaB and IL-8 in human intestinal epithelial cells. American journal of physiology. Gastrointestinal and liver physiology 42 17540779
2018 A CARD9 Founder Mutation Disrupts NF-κB Signaling by Inhibiting BCL10 and MALT1 Recruitment and Signalosome Formation. Frontiers in immunology 41 30429846
2011 The E3 ubiquitin ligase mind bomb-2 (MIB2) protein controls B-cell CLL/lymphoma 10 (BCL10)-dependent NF-κB activation. The Journal of biological chemistry 41 21896478
2007 Post-translational modifications regulate distinct functions of CARMA1 and BCL10. Trends in immunology 40 17468049
2005 A pathway for tumor necrosis factor-alpha-induced Bcl10 nuclear translocation. Bcl10 is up-regulated by NF-kappaB and phosphorylated by Akt1 and then complexes with Bcl3 to enter the nucleus. The Journal of biological chemistry 39 16280327
2010 Lipopolysaccharide-induced activation of NF-κB non-canonical pathway requires BCL10 serine 138 and NIK phosphorylations. Experimental cell research 38 20466000
2002 Protein kinase C-associated kinase (PKK) mediates Bcl10-independent NF-kappa B activation induced by phorbol ester. The Journal of biological chemistry 37 12091384
2014 T cell receptor signals to NF-κB are transmitted by a cytosolic p62-Bcl10-Malt1-IKK signalosome. Science signaling 36 24825920
2006 Bcl10 is phosphorylated on Ser138 by Ca2+/calmodulin-dependent protein kinase II. Molecular immunology 36 17052756
2007 Bcl10 plays a divergent role in NK cell-mediated cytotoxicity and cytokine generation. Journal of immunology (Baltimore, Md. : 1950) 35 17785812
2008 Multiple protein domains mediate interaction between Bcl10 and MALT1. The Journal of biological chemistry 34 18806265
2007 Phosphorylation of Bcl10 negatively regulates T-cell receptor-mediated NF-kappaB activation. Molecular and cellular biology 34 17502353
2005 MALT1 contains nuclear export signals and regulates cytoplasmic localization of BCL10. Blood 34 16123224
2018 Ubiquitination and phosphorylation of the CARD11-BCL10-MALT1 signalosome in T cells. Cellular immunology 33 30514565
2008 Loss of protein kinase C theta, Bcl10, or Malt1 selectively impairs proliferation and NF-kappa B activation in the CD4+ T cell subset. Journal of immunology (Baltimore, Md. : 1950) 31 18941215
2004 No evidence of a correlation between BCL10 expression and API2-MALT1 gene rearrangement in ocular adnexal MALT lymphoma. Pathology international 30 14674990
1999 Bcl10 is not a target for frequent mutation in human carcinomas. British journal of cancer 30 10408401
1999 Point mutations and deletions of the Bcl10 gene in solid tumors and malignant lymphomas. Cancer research 30 10582682
2009 COP9 signalosome controls the Carma1-Bcl10-Malt1 complex upon T-cell stimulation. EMBO reports 29 19444310
2008 Lipopolysaccharide activates NF-kappaB by TLR4-Bcl10-dependent and independent pathways in colonic epithelial cells. American journal of physiology. Gastrointestinal and liver physiology 29 18718996
2018 GSK3β modulates NF-κB activation and RelB degradation through site-specific phosphorylation of BCL10. Scientific reports 28 29358699
2011 CaMKII targets Bcl10 in T-cell receptor induced activation of NF-κB. Molecular immunology 27 21513986
2006 Nuclear bcl10 expression characterizes a group of ocular adnexa MALT lymphomas with shorter failure-free survival. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 27 16648871
2006 Aberrant nuclear BCL10 expression and lack of t(11;18)(q21;q21) in primary cutaneous marginal zone B-cell lymphoma. Human pathology 27 16784987
2022 BCL10 Mutations Define Distinct Dependencies Guiding Precision Therapy for DLBCL. Cancer discovery 26 35658124
1999 Lack of Bcl10 mutations in testicular germ cell tumours and derived cell lines. British journal of cancer 26 10408400
2018 Ancient Origin of the CARD-Coiled Coil/Bcl10/MALT1-Like Paracaspase Signaling Complex Indicates Unknown Critical Functions. Frontiers in immunology 25 29881386
1999 Mutations in Bcl10 are very rare in colorectal cancer. British journal of cancer 24 10408399
2019 Bcl10 is required for the development and suppressive function of Foxp3+ regulatory T cells. Cellular & molecular immunology 22 31595055
2014 Bcl10 mediates angiotensin II-induced cardiac damage and electrical remodeling. Hypertension (Dallas, Tex. : 1979) 22 25185127

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