Affinage

CD79B

B-cell antigen receptor complex-associated protein beta chain · UniProt P40259

Length
229 aa
Mass
26.0 kDa
Annotated
2026-04-28
100 papers in source corpus 33 papers cited in narrative 33 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD79B (Igβ/B29) is a B-cell-specific transmembrane signaling subunit of the B cell antigen receptor (BCR) that orchestrates receptor assembly, signal transduction, internalization, and B cell fate decisions from the earliest stages of B cell development through terminal differentiation. CD79B forms a disulfide-linked heterodimer with CD79A (Igα), and this heterodimer is essential for BCR surface expression by chaperoning immunoglobulin through N-glycan maturation in the ER; loss of CD79B or disruption of the CD79A–CD79B disulfide bond (e.g., the G137S mutation that causes agammaglobulinemia) traps immature BCR in the ER (PMID:36426942, PMID:17675462, PMID:17709424). Upon antigen engagement, dual ITAM phosphorylation on CD79B recruits Syk kinase and couples to Src-family kinases (Lyn, Blk, Fyn), PI3K, Ca²⁺ flux, ERK/MAPK, and AKT pathways to drive activation and antigen presentation trafficking to late endosomes, while monophosphorylation of the ITAM instead recruits SHIP-1/Dok-1 to enforce B cell anergy (PMID:8580068, PMID:16818674, PMID:22078222, PMID:10352267). Gain-of-function CD79B ITAM mutations—particularly Y196 variants—cooperate with MYD88(L265P) to constitutively activate NF-κB, block peripheral B cell deletion, and drive lymphomagenesis in diffuse large B cell lymphoma (PMID:28701369, PMID:26111727).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1988 High

    Identification of CD79B as a novel B-cell-specific gene encoding a transmembrane Ig superfamily protein expressed from the earliest B cell precursors established the existence of a dedicated signaling component distinct from membrane immunoglobulin itself.

    Evidence cDNA cloning and genomic sequencing from B cell libraries

    PMID:3137575

    Open questions at the time
    • No binding partner or receptor association defined
    • Function unknown beyond expression pattern
  2. 1991 High

    Biochemical identification of CD79B and CD79A as components of the IgM antigen receptor complex resolved the long-standing question of how membrane immunoglobulin, which has a minimal cytoplasmic tail, could transduce signals.

    Evidence Immunoprecipitation, amino-terminal sequencing, and immunoblotting of IgM-associated phosphoproteins

    PMID:2023945

    Open questions at the time
    • Stoichiometry of complex unknown
    • Nature of association (covalent vs. noncovalent) unresolved
  3. 1992 High

    Demonstration that CD79B forms a disulfide-linked heterodimer with CD79A that noncovalently associates with surface IgM, and that the heterodimer physically couples to Src-family kinases (Blk, Lyn, Fyn), defined the molecular architecture linking antigen recognition to intracellular signaling.

    Evidence Co-precipitation, co-capping, SDS-PAGE under reducing/non-reducing conditions, and detergent dissociation kinase assays

    PMID:1506682 PMID:1731334

    Open questions at the time
    • Which ITAM residues mediate kinase coupling not determined
    • Individual contributions of CD79A vs. CD79B to signaling unclear
  4. 1993 High

    Functional dissection revealed that CD79B ITAM is sufficient for Ca²⁺ signaling and is the preferred ligand for Syk kinase SH2 domains, while a C-terminally truncated splice variant lacking phosphorylatable residues exists in specific B cell subsets, establishing that CD79B has a non-redundant signaling role distinct from CD79A.

    Evidence Chimeric receptor reconstitution with mutagenesis, in vitro SH2 binding assays, anti-Igβ cross-linking with Ca²⁺/phosphorylation readouts, and N-terminal sequencing of truncated protein

    PMID:7688784 PMID:8268137 PMID:8454858 PMID:8580068

    Open questions at the time
    • Downstream targets of Syk recruited via CD79B ITAM not mapped
    • Physiological role of truncated variant in B cell regulation unclear
  5. 1997 High

    In vivo genetic studies established that CD79B ITAM signaling drives pro-B to pre-B cell differentiation and allelic exclusion, demonstrating that CD79B is not merely an accessory but is required for B cell developmental checkpoints.

    Evidence Anti-Igβ cross-linking on RAG-2-deficient pro-B cells with differentiation readout; transgenic mice expressing IgM/Igβ chimeric receptors with ITAM mutations

    PMID:9151700 PMID:9354476

    Open questions at the time
    • Whether CD79B has roles independent of CD79A in vivo not resolved
    • Mechanism of allelic exclusion signaling downstream of ITAM not defined
  6. 1999 High

    Studies of BCR dynamics, trafficking, and transcriptional regulation revealed that CD79A/CD79B heterodimer integrity is required for BCR trafficking to late endosomes and antigen presentation, that antigen stimulation destabilizes the mIg–CD79A/CD79B complex as a desensitization mechanism, and that CD79B transcription is activated by EBF through promoter-proximal sites.

    Evidence Chimeric BCR constructs with antigen presentation assays; co-IP after stimulation with kinase inhibitor controls; promoter reporter assays with EBF and linker-scanning mutagenesis

    PMID:10072076 PMID:10352267 PMID:9858563

    Open questions at the time
    • Structural basis of mIg–CD79A/CD79B destabilization unknown
    • Whether BCR desensitization occurs in vivo during immune responses not shown
  7. 1999 High

    Discovery of the alternatively spliced ΔCD79b transcript (lacking the Ig-like domain) in CLL revealed a potential disease mechanism: overexpression of ΔCD79b reduces surface BCR and blocks BCR-mediated apoptosis, acting as a dominant-negative by retaining IgM in the ER.

    Evidence RT-PCR quantification in CLL cohort; transfection of ΔCD79b into Ramos cells with apoptosis assay and leader/ITAM mutagenesis; co-IP and ER retention studies in 293T cells

    PMID:10090943 PMID:12115635 PMID:12384401

    Open questions at the time
    • Mechanism of alternative splicing regulation not identified
    • Whether ΔCD79b contributes to CLL pathogenesis beyond correlation not established in vivo
  8. 2001 High

    Epistatic genetic studies showed that combined loss of CD79A ITAM phosphorylation and CD79B cytoplasmic function completely blocks B cell development, and that BTK acts downstream of CD79B for pro-B to pre-B transition, placing CD79B in a defined signaling hierarchy.

    Evidence CD79α ITAM Tyr→Phe knock-in combined with CD79β cytoplasmic truncation in mice; RAG2/BTK double-knockout with CD79b cross-linking

    PMID:11282988 PMID:11514602

    Open questions at the time
    • How BTK is specifically activated by CD79B-initiated signals vs. CD79A not resolved
    • Whether the complete developmental block is solely ITAM-dependent not tested
  9. 2006 High

    Knock-in replacement of CD79B ITAM tyrosines with alanines uncoupled internalization from downstream signaling: mutant B cells showed decreased BCR internalization yet paradoxically enhanced and prolonged Ca²⁺, AKT, and ERK signaling, establishing that CD79B ITAM tyrosines serve a dual role as both activation initiators and negative regulators via receptor downmodulation.

    Evidence Igβ ITAM Tyr→Ala knock-in mice with BCR internalization assays, Ca²⁺ flux, pAKT, and pERK measurements

    PMID:16818674

    Open questions at the time
    • Identity of the ubiquitin ligase or endocytic adaptor recruited by phospho-ITAM for internalization unknown
    • Whether enhanced signaling leads to autoimmunity in aged mice not reported
  10. 2007 High

    Identification of human CD79B loss-of-function mutations (a nonsense mutation and a hypomorphic G137S missense near the disulfide bond cysteine) causing agammaglobulinemia established CD79B as a Mendelian disease gene and confirmed that CD79A–CD79B heterodimerization is essential for BCR surface expression in humans.

    Evidence Patient mutation identification, heterologous expression in Drosophila S2 and 293T/Jurkat cells with co-association and surface expression assays

    PMID:17675462 PMID:17709424

    Open questions at the time
    • Frequency of CD79B mutations among agammaglobulinemia patients not fully defined
    • Whether residual non-BCR signaling occurs in CD79B-null human B cells unknown
  11. 2011 High

    The discovery that ITAM monophosphorylation on CD79B recruits SHIP-1/Dok-1 to enforce B cell anergy—while dual phosphorylation drives activation—resolved how a single motif generates opposing signaling outcomes and linked this switch to autoimmune prevention.

    Evidence Conditional SHIP-1 knockout mice with constitutive ITAM monophosphorylation analysis, BCR signaling assays, and autoantibody measurements

    PMID:22078222

    Open questions at the time
    • Structural basis for how monophosphorylation vs. diphosphorylation recruits distinct effectors not determined
    • Whether SHIP-1 binds directly to monophospho-CD79B or indirectly via adaptors not clarified
  12. 2015 Medium

    Systematic sequencing of DLBCL revealed that CD79B ITAM mutations (especially Y196) recurrently activate NF-κB and frequently co-occur with MYD88 mutations, suggesting cooperative oncogenic signaling; separately, CD79B overexpression was shown to confer ibrutinib resistance via AKT/MAPK activation.

    Evidence Sequencing of NF-κB pathway genes in 71 PCNSL cases; CD79B overexpression/knockdown with ibrutinib sensitivity and pAKT/pMAPK assays in ABC-DLBCL lines

    PMID:26111727 PMID:26699656

    Open questions at the time
    • Direct demonstration that CD79B Y196 mutation activates NF-κB in a reconstituted system not shown in these studies
    • Mechanism by which CD79B overexpression bypasses BTK inhibition at the molecular level not defined
  13. 2017 High

    Functional reconstitution demonstrated that CD79B and MYD88(L265P) mutations cooperate to block peripheral B cell deletion and trigger plasmablast differentiation: CD79B mutations alone increase surface IgM while MYD88 alone causes intracellular IgM retention resembling anergy, but the combination escapes tolerance and drives autoantibody secretion.

    Evidence Retroviral expression of mutant CD79B and MYD88 in normal mouse B cells with surface IgM, endoglycosidase H, survival/proliferation, and in vivo peripheral deletion assays

    PMID:28701369

    Open questions at the time
    • Whether the cooperative mechanism involves direct physical interaction between CD79B and MYD88 signaling complexes unknown
    • Relevance to initial lymphoma-initiating events vs. tumor maintenance not distinguished
  14. 2018 High

    CRISPR deletion experiments revealed that CD79B can signal independently of the full BCR by forming a surface complex with CD19 in Burkitt lymphoma cells, establishing a BCR-independent survival signaling module that still depends on the CD79B ITAM.

    Evidence CRISPR/Cas9 knockout of BCR components in Ramos cells, competitive growth assay, proximity ligation assay for CD79B–CD19

    PMID:29669863

    Open questions at the time
    • Whether the CD79B–CD19 module exists in normal B cells or is lymphoma-specific unknown
    • Downstream signaling effectors of CD79B–CD19 not mapped
  15. 2022 High

    CRISPR knockout and rescue experiments definitively demonstrated that CD79B is required for BCR N-glycan maturation and ER exit, and that the agammaglobulinemia-associated G137S mutant fails to rescue because it cannot form the critical CD79A–CD79B disulfide-linked heterodimer.

    Evidence CRISPR/Cas9 CD79B KO in B lymphoma lines with wild-type and G137S rescue, endoglycosidase H sensitivity assay, flow cytometry

    PMID:36426942

    Open questions at the time
    • ER quality control machinery recognizing unpaired CD79A not identified
    • Whether chaperone interactions differ for wild-type vs. G137S CD79B not examined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for how ITAM mono- vs. di-phosphorylation switches between SHIP-1-mediated anergy and Syk-mediated activation, the molecular mechanism by which CD79B–CD19 signals independently of the BCR, and how CD79B cooperates with MYD88 at the level of signalosome assembly to drive lymphomagenesis.
  • No high-resolution structure of the CD79A–CD79B heterodimer or its ITAM phosphoforms with effectors
  • Molecular basis of CD79B–CD19 interaction and signaling unknown
  • Direct signalosome composition linking CD79B mutants to MYD88-dependent NF-κB not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 6 GO:0060090 molecular adaptor activity 3
Localization
GO:0005886 plasma membrane 5 GO:0005783 endoplasmic reticulum 2 GO:0005768 endosome 1
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-168256 Immune System 6 R-HSA-1266738 Developmental Biology 5 R-HSA-1643685 Disease 3 R-HSA-9609507 Protein localization 3
Partners
BLKBTKCD19CD79AFYNLYNSHIP1SYK
Complex memberships
BCR (B cell antigen receptor complex)CD79A-CD79B (Igα/Igβ) heterodimerCD79B-CD19 signaling module

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 CD79B (B29) encodes a B-cell-specific transmembrane protein with a single extracellular immunoglobulin-like domain, a hydrophobic transmembrane segment, and a charged intracytoplasmic domain, expressed at all stages of B-cell development beginning with the earliest precursor B cells. cDNA cloning, genomic sequencing, structural domain analysis Proceedings of the National Academy of Sciences of the United States of America High 3137575
1991 CD79B (B29) protein and mb-1 (CD79a) gene products are components of the membrane IgM antigen receptor complex; B29 and mb-1 products form the Ig-beta/Ig-gamma and Ig-alpha chains, respectively, of the IgM-associated phosphoprotein complex, identified by amino-terminal sequencing and immunoblotting. Immunoprecipitation, proteolytic peptide mapping, amino-terminal sequencing, immunoblotting Proceedings of the National Academy of Sciences of the United States of America High 2023945
1992 CD79B (B29) protein is disulfide-linked in a heterodimer with the mb-1 (CD79a) protein, and this heterodimer is noncovalently associated with surface IgM on B lymphocytes; surface expression of B29 correlates directly with surface mu heavy-chain density. Antibody precipitation, co-capping experiments, SDS-PAGE, immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 1731334
1992 The MB-1/B29 (CD79a/CD79b) heterodimer physically couples the B cell antigen receptor to multiple Src-family protein tyrosine kinases (Blk, Lyn, Fyn); disruption of mIg–MB-1/B29 association with NP-40 abolishes tyrosine kinase activity from mIg, while MB-1/B29 retains kinase association. Co-immunoprecipitation under different detergent conditions (digitonin vs. NP-40), kinase activity assay Journal of immunology High 1506682
1993 Signal transduction by membrane immunoglobulin is mediated through Igα (CD79a) and Igβ (CD79b): specific transmembrane mutations in Ig that abolish Ca2+ and phosphorylation responses also uncouple IgM from Igα/Igβ; cytoplasmic domain fusions restore activity, with Igα sufficient for both Ca2+ and phosphorylation and Igβ sufficient only for Ca2+ responses. Mutagenesis of Ig transmembrane domain, Ca2+ flux assay, phosphorylation assay, chimeric receptor reconstitution The Journal of experimental medicine High 7688784
1993 Tyrosine-phosphorylated CD79b (Igβ) is a major ligand for the tandem SH2 domains of Syk kinase in activated B cells, with binding occurring predominantly via Igβ rather than Igα, suggesting the two receptor components couple to distinct signaling pathways. In vitro SH2 domain binding assay, immunoprecipitation from activated B cell lysates, protein identification International immunology High 8580068
1993 Cross-linking of CD79b (Igβ) on human B cells activates tyrosine kinases, induces phosphatidylinositide hydrolysis, and elevates intracellular Ca2+, demonstrating that Igβ ligation initiates signal transduction pathways qualitatively identical to anti-μ stimulation; anti-Igβ antibodies also modulate BCR and block plasma cell terminal differentiation. Anti-Igβ antibody cross-linking, tyrosine kinase activation assay, intracellular Ca2+ measurement, phosphatidylinositide hydrolysis assay International immunology High 8268137
1993 The Igβ (Ig-gamma) chain is a C-terminally truncated product of the B29 gene lacking the 30–36 C-terminal residues encoded by the most 3' exon; this truncated form is not phosphorylatable and is found in intermediate/low density splenic B cells but not resting B cells. N-terminal sequencing, immunoblotting, immunoprecipitation, peptide antiserum Journal of immunology High 8454858
1993 Both Igα and Igβ are required for Ig-mediated antigen-induced apoptosis in immature B cells; heterodimers of Igα and Igβ efficiently induced apoptosis while homodimers of either chain alone did not, associated with restricted tyrosine phosphorylation including Syk. Chimeric receptor dimer formation, receptor aggregation, apoptosis assay (WEHI-231 cells), tyrosine phosphorylation analysis Blood High 9057631
1997 Cross-linking of CD79b (Igβ) on pro-B cells from RAG-2-deficient mice induces rapid tyrosine-phosphorylation of Igα and intracellular proteins including Syk, PI3-kinase, Vav, SLP-76, and ERK activation, and drives differentiation of developmentally arrested pro-B cells to the small pre-B cell stage. Anti-Igβ monoclonal antibody cross-linking, immunofluorescence, phosphorylation assays, in vivo antibody treatment of RAG-2-deficient mice Immunity High 9354476
1997 The cytoplasmic domains of Igα and Igβ (CD79b) are each independently sufficient to mediate allelic exclusion, rescue B cell development in Igμ-deficient mice, and signal B7 upregulation via their ITAMs, though Igα/Igβ together give optimal activity. Transgenic mice expressing IgM/Igα and IgM/Igβ chimeric receptors, ITAM mutation, B cell development analysis The Journal of experimental medicine High 9151700
1999 Antigen stimulation leads to dissociation of the BCR reflected by inability to co-immunoprecipitate Igα/Igβ with mIg, temporally correlated with receptor desensitization; this destabilization requires tyrosine kinase activation, occurs at the cell surface, and 'dissociated' Igα/Igβ complexes remain responsive to anti-Igβ stimulation. Co-immunoprecipitation, receptor desensitization assay, tyrosine kinase inhibitor treatment Immunity High 10072076
1999 Both Igα and Igβ (CD79b) are required for efficient BCR trafficking to late endosomes (MIIC compartment) and enhancement of antigen presentation; chimeric complexes containing either chain alone fail to access MIIC or enhance antigen presentation, and ITAM tyrosine mutation in Igα also abolishes MIIC access. Chimeric BCR constructs, antigen presentation assay, subcellular localization by microscopy Journal of immunology High 10352267
1999 The B29 (CD79b) gene is a transcriptional target of the Early B-cell Factor (EBF) transcription factor; EBF interacts with three independent sites within the B29 promoter and activates B29 promoter-driven reporter and endogenous B29 gene expression; EBF binding site mutations diminish B29 promoter activity in pre-B cells. Promoter reporter assay, EBF ectopic expression in HeLa cells, linker scanning mutagenesis, EMSA Molecular and cellular biology High 9858563
1999 An alternatively spliced form of CD79b (ΔCD79b) lacking the extracellular Ig-like domain (exon 3) is present in normal and CLL B cells and is increased in CLL relative to full-length CD79b; this alternative splicing, not point mutations in exon 3, accounts for reduced BCR surface expression in most CLL cases. RT-PCR, radioactive PCR quantification, direct sequencing, SSCP analysis Blood High 10090943
2000 B29 (CD79b) mutations found in CLL affect BCR signaling: a transmembrane domain truncation mutant fails to associate with μ or mb-1 at the cell surface, while a cytoplasmic ITAM-truncating mutant allows surface expression but shows significant impairment of anti-IgM-stimulated MAPK activation. Vaccinia virus expression system in Jurkat T cells reconstituted with BCR components, co-immunoprecipitation, MAPK activation assay Proceedings of the National Academy of Sciences of the United States of America High 10792036
2001 Igα (CD79a) ITAM tyrosine phosphorylation is required for B1 and marginal zone B cell development; when combined with Igβ (CD79b) cytoplasmic domain truncation, B cell development is completely blocked at the pro-B cell stage, demonstrating a crucial and cooperative role for both ITAM phosphorylations. Gene targeting (knock-in of Igα ITAM Tyr→Phe and Igβ truncation), B cell developmental analysis in mice The Journal of experimental medicine High 11514602
2002 The alternatively spliced ΔCD79b transcript is expressed as protein, and its overexpression in Ramos-EHRB cells transforms them from BCR apoptosis-sensitive to highly resistant; inhibitory activity requires an intact leader sequence for ER trafficking and a functional ITAM in its cytoplasmic tail. Transfection of ΔCD79b into B lymphoma cells, apoptosis assay (anti-Fcμ), leader sequence and ITAM mutagenesis Blood High 12384401
2002 Bob1 (OCA-B/OBF-1) differentially transactivates the B29 (CD79b) but not the mb-1 (CD79a) promoter through an octamer motif with adenosine at position 5; swapping octamer motifs between the two promoters transfers Bob1 responsiveness, and Bob1 can override B29 silencer activity. Promoter reporter assay, Bob1 cotransfection, octamer motif swapping mutagenesis Journal of immunology High 11907094
2003 CD79b (B29) and CD79a (mb-1) genes undergo somatic hypermutation in germinal center and post-GC B cells at frequencies similar to other non-Ig genes; B29 mutations display a bimodal distribution resembling CD95/Fas, with distal cytoplasmic domain mutations potentially limiting BCR signaling and contributing to B cell survival. Sequencing of B29 and mb-1 genes from GC-derived malignant B cell lines and normal peripheral B cells, mutation frequency and distribution analysis Proceedings of the National Academy of Sciences of the United States of America High 12651942
2006 Igβ (CD79b) ITAM tyrosine residues regulate BCR internalization: mice with Igβ ITAM tyrosines replaced by alanine show decreased steady-state and ligand-mediated BCR internalization, higher surface IgM/IgD levels, decreased Src and Syk activation, but paradoxically enhanced and prolonged downstream BCR signaling (Ca2+ flux, AKT, ERK) and enhanced T-independent antigen responses. Gene targeting (Igβ ITAM Tyr→Ala knock-in), BCR internalization assay, flow cytometry, kinase activation assays, Ca2+ flux The Journal of experimental medicine High 16818674
2007 A homozygous nonsense mutation in Igβ (CD79b) causes agammaglobulinemia in humans due to complete block of B cell development at the pro-B to pre-B transition; the mutant Igβ cannot associate with Igα (shown by transfection in Drosophila S2 cells), and BCR complex assembly on the cell surface is abrogated. Patient mutation identification, transfection in Drosophila S2 cells, co-association assay, bone marrow immunofluorescence The Journal of experimental medicine High 17709424
2007 A hypomorphic missense mutation in Igβ (CD79b; G137S, adjacent to the Igα/Igβ disulfide bond cysteine) impairs but does not abolish disulfide-linked complex formation with Igα and surface BCR assembly, resulting in a leaky B cell developmental defect with very few surface IgM-dim B cells. Expression vectors in 293T and Jurkat cells, disulfide-linked complex assay, flow cytometry of patient B cells Journal of immunology High 17675462
2011 Monophosphorylation of CD79b (and CD79a) ITAM motifs (rather than dual phosphorylation) initiates an inhibitory signaling cascade via SHIP-1 and its adaptor Dok-1, which are constitutively phosphorylated in anergic B cells; B cell-targeted SHIP-1 deletion abolishes anergy, restores BCR signaling, and causes lupus-like disease. Conditional SHIP-1 knockout mice, phosphorylation analysis, BCR signaling assays, autoantibody measurement, Src-family kinase inhibition Immunity High 22078222
2013 IL-4 markedly upregulates Igα and Igβ (CD79b) protein expression (requiring STAT6) in primary B cells; elevated Igα/Igβ form heterodimers that associate with IgM, promote IgM maturation and surface expression, and amplify BCR-initiated signaling in a Lyn-dependent manner. Western blot, STAT6 knockout, co-immunoprecipitation, surface IgM quantification, BCR signaling (pERK), in vivo IL-4 neutralization Journal of immunology High 23776171
2001 BTK is required for CD79b-mediated pro-B to pre-B cell transition: pro-B cells from RAG2/BTK double-knockout mice fail to differentiate after CD79b cross-linking, despite normal Erk1/2 and PLCγ2 phosphorylation; BTK is itself phosphorylated after CD79b cross-linking on RAG2-deficient pro-B cells. RAG2/BTK double-knockout mice, CD79b cross-linking, differentiation assay, phosphorylation analysis International immunology High 11282988
2018 CD79b (Igβ) is required for the fitness and competitive growth of Burkitt lymphoma (Ramos) B cells; in the absence of other BCR components, Igβ can be expressed on the B cell surface in close proximity to CD19, signaling in an ITAM-dependent manner, forming an alternative B-cell signaling module with CD19. CRISPR/Cas9 deletion of BCR genes in Ramos cells, competitive growth assay, proximity ligation assay, ITAM-dependent signaling analysis The EMBO journal High 29669863
2017 CD79B mutations alone increase surface IgM but do not enhance B cell survival/proliferation; MYD88(L265P) alone decreases surface IgM via intracellular IgM retention resembling anergic trafficking; combined CD79B and MYD88 mutations, but not individually, block peripheral deletion and trigger plasmablast differentiation and autoantibody secretion in self-antigen-stimulated B cells. Retroviral expression of CD79B and MYD88 mutants in normal activated mouse B lymphocytes, surface IgM flow cytometry, endoglycosidase H sensitivity assay, survival/proliferation assays, in vivo peripheral deletion assay The Journal of experimental medicine High 28701369
2015 CD79B mutations (predominantly Y196 in the ITAM domain) activate NF-κB signaling and are recurrent in primary CNS DLBCL (83% frequency) and frequently co-occur with MYD88 mutations, suggesting cooperative constitutive activation of BCR and MYD88 signaling pathways in immune-privileged sites. Systematic sequencing of 21 NF-κB-relevant genes in 71 PCNSL cases plus pyrosequencing validation Neuropathology and applied neurobiology Medium 26111727
2022 Deletion of CD79B (or CD79A) by CRISPR/Cas9 in human B lymphoma cell lines causes loss of surface IgM and a block in N-glycan maturation with accumulation of immature BCR proteins in the ER; rescue with wild-type CD79B restores surface CD79A and IgM with mature glycosylation, whereas the naturally occurring CD79B G137S mutant (which disrupts CD79A/CD79B heterodimerization) does not rescue. CRISPR/Cas9 knockout, rescue transfection with wild-type and G137S CD79B, endoglycosidase H glycosylation assay, flow cytometry, Western blot Journal of immunology High 36426942
2015 CD79B overexpression confers resistance to ibrutinib in ABC-DLBCL by activating AKT and MAPK signaling as an alternative pathway; CD79B depletion sensitizes primary refractory cells to ibrutinib and reduces AKT/MAPK phosphorylation; combination of AKT or MAPK inhibitors with ibrutinib circumvents resistance. cDNA microarray, Western blot, CD79B overexpression and knockdown, ibrutinib sensitivity assay, AKT/MAPK phosphorylation analysis Leukemia & lymphoma Medium 26699656
2011 CD79b (Igβ) protein expression in plasma cell myeloma is downregulated at the post-transcriptional level: CD79b mRNA transcripts are detectable by RT-PCR in myeloma cell lines, but CD79b protein is absent by immunohistochemistry and Western blot, indicating post-transcriptional regulation. RT-PCR, Western blot, immunohistochemistry in PCM cell lines and clinical samples Pathology international Medium 21355953
2002 Alternatively spliced forms of Igα and Igβ (ΔIgα, ΔIgβ) that lack the Ig-like extracellular domain do not form heterodimers with their full-length counterparts, do not mediate IgM transport to the cell surface, and when overexpressed act as dominant-negative competitors retaining IgM in the ER. cDNA transfection in 293T cells, co-immunoprecipitation, surface IgM flow cytometry, ER retention assay European journal of immunology High 12115635

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Improvement of the chronic lymphocytic leukemia scoring system with the monoclonal antibody SN8 (CD79b). American journal of clinical pathology 272 9322589
2015 Safety and activity of the anti-CD79B antibody-drug conjugate polatuzumab vedotin in relapsed or refractory B-cell non-Hodgkin lymphoma and chronic lymphocytic leukaemia: a phase 1 study. The Lancet. Oncology 270 25925619
2009 Therapeutic potential of an anti-CD79b antibody-drug conjugate, anti-CD79b-vc-MMAE, for the treatment of non-Hodgkin lymphoma. Blood 227 19633198
1988 B29: a member of the immunoglobulin gene superfamily exclusively expressed on beta-lineage cells. Proceedings of the National Academy of Sciences of the United States of America 210 3137575
1993 Signal transduction by immunoglobulin is mediated through Ig alpha and Ig beta. The Journal of experimental medicine 204 7688784
1991 X-ray analysis of the single chain B29-A1 peptide-linked insulin molecule. A completely inactive analogue. Journal of molecular biology 191 1856866
2015 Recurrent mutations of CD79B and MYD88 are the hallmark of primary central nervous system lymphomas. Neuropathology and applied neurobiology 185 26111727
2013 High prevalence of oncogenic MYD88 and CD79B mutations in diffuse large B-cell lymphomas presenting at immune-privileged sites. Blood cancer journal 165 24013661
2011 Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy. Immunity 139 22078222
1991 IgM antigen receptor complex contains phosphoprotein products of B29 and mb-1 genes. Proceedings of the National Academy of Sciences of the United States of America 135 2023945
2015 Anti-CD22 and anti-CD79B antibody drug conjugates are active in different molecular diffuse large B-cell lymphoma subtypes. Leukemia 126 25708834
2003 Somatic hypermutation of the B cell receptor genes B29 (Igbeta, CD79b) and mb1 (Igalpha, CD79a). Proceedings of the National Academy of Sciences of the United States of America 106 12651942
1992 The MB-1/B29 heterodimer couples the B cell antigen receptor to multiple src family protein tyrosine kinases. Journal of immunology (Baltimore, Md. : 1950) 98 1506682
1997 The Ig alpha/Igbeta heterodimer on mu-negative proB cells is competent for transducing signals to induce early B cell differentiation. Immunity 90 9354476
2001 Interference with immunoglobulin (Ig)alpha immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation modulates or blocks B cell development, depending on the availability of an Igbeta cytoplasmic tail. The Journal of experimental medicine 86 11514602
1989 Immunoglobulin enhancer and promoter motifs 5' of the B29 B-cell-specific gene. Proceedings of the National Academy of Sciences of the United States of America 86 2508087
1999 Antigen-stimulated dissociation of BCR mIg from Ig-alpha/Ig-beta: implications for receptor desensitization. Immunity 74 10072076
1999 An alternatively spliced form of CD79b gene may account for altered B-cell receptor expression in B-chronic lymphocytic leukemia. Blood 73 10090943
2015 Primary diffuse large B-cell lymphomas of central nervous system exhibit remarkably high prevalence of oncogenic MYD88 and CD79B mutations. Leukemia & lymphoma 72 25347427
2019 Chimeric Antigen Receptor T Cells Targeting CD79b Show Efficacy in Lymphoma with or without Cotargeting CD19. Clinical cancer research : an official journal of the American Association for Cancer Research 67 31439577
2006 Ig beta tyrosine residues contribute to the control of B cell receptor signaling by regulating receptor internalization. The Journal of experimental medicine 67 16818674
1996 Expression of the immunoglobulin-associated protein B29 in B cell disorders with the monoclonal antibody SN8 (CD79b). Leukemia 67 8946938
1997 Aberrations of the B-cell receptor B29 (CD79b) gene in chronic lymphocytic leukemia. Blood 66 9269755
1992 The B29 and mb-1 polypeptides are differentially expressed during human B cell differentiation. European journal of immunology 66 1396979
2018 Continuous signaling of CD79b and CD19 is required for the fitness of Burkitt lymphoma B cells. The EMBO journal 62 29669863
1993 Multiple motifs regulate the B-cell-specific promoter of the B29 gene. Proceedings of the National Academy of Sciences of the United States of America 62 8265616
2023 B-Cell Receptor Signaling and Beyond: The Role of Igα (CD79a)/Igβ (CD79b) in Normal and Malignant B Cells. International journal of molecular sciences 58 38203179
2007 Mutations of the Igbeta gene cause agammaglobulinemia in man. The Journal of experimental medicine 54 17709424
2002 Inotropic responses to human gene 2 (B29) relaxin in a rat model of myocardial infarction (MI): effect of pertussis toxin. British journal of pharmacology 54 12381685
2016 Frequent MYD88 L265P and CD79B Mutations in Primary Breast Diffuse Large B-Cell Lymphoma. The American journal of surgical pathology 51 26752547
1999 The B29 (immunoglobulin beta-chain) gene is a genetic target for early B-cell factor. Molecular and cellular biology 50 9858563
1999 Quantitative analysis of CD79b, CD5 and CD19 in mature B-cell lymphoproliferative disorders. Haematologica 49 10329919
1997 The immunoglobulin (Ig)alpha and Igbeta cytoplasmic domains are independently sufficient to signal B cell maturation and activation in transgenic mice. The Journal of experimental medicine 49 9151700
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