Affinage

CD79B

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

Length
229 aa
Mass
26.0 kDa
Annotated
2026-06-09
100 papers in source corpus 41 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD79B (Ig-beta/B29) is a transmembrane signaling subunit of the B cell antigen receptor (BCR) that, together with CD79A (Ig-alpha), forms the obligate heterodimer required for surface IgM assembly and signal transduction (PMID:2269334, PMID:1373499, PMID:7688784). The two chains are joined by an intermolecular disulfide bond between Ig-alpha C113 and Ig-beta C135, and this covalent linkage is required for efficient BCR assembly and surface delivery; CD79B loss causes ER retention of immature, endoglycosidase H-sensitive BCR components, and disulfide-disrupting mutations such as G137S abolish heterodimerization and surface IgM (PMID:16877534, PMID:36426942). Through its cytoplasmic ITAM, CD79B recruits a distinct effector repertoire from CD79A — associating with PI3K rather than Lyn/Fyn — and its tyrosine-phosphorylated ITAM binds the tandem SH2 domains of Syk to drive Syk autophosphorylation and activation (PMID:1439759, PMID:7538118, PMID:8580068). CD79B ITAM tyrosines transduce antigen-independent developmental signals that require BTK and drive the pro-B to pre-B transition, V(D)J recombination, and allelic exclusion, functioning with partial redundancy alongside the Ig-alpha ITAM (PMID:7716544, PMID:8602530, PMID:11514602, PMID:11282988); loss-of-function CD79B mutations cause human agammaglobulinemia with a block at the pro-B to pre-B transition (PMID:17709424). Beyond receptor assembly, CD79B sets BCR signaling thresholds and routes antigen for presentation: its ITAM tyrosines regulate steady-state and ligand-induced BCR internalization (PMID:16818674), Itch-dependent diubiquitinylation directs endosomal sorting and antigen presentation (PMID:17878339), and Ig-beta-specific PI3K activation in endocytic compartments builds the multivesicular antigen-processing compartment (PMID:12459553). ITAM monophosphorylation in anergic B cells engages an inhibitory SHIP-1/Dok-1 circuit that enforces tolerance (PMID:22078222). In malignancy, an alternatively spliced exon-3-deleted variant acts as a dominant-negative regulator of surface BCR in CLL (PMID:12384401, PMID:12115635), while ITAM Y196 hotspot mutations cooperate with MYD88 mutations to activate NF-kB, block peripheral B cell deletion, and drive lymphomagenesis at immune-privileged sites (PMID:28701369, PMID:26111727).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1990 High

    Established that CD79B is a physical component of the BCR, answering whether surface IgM required dedicated accessory chains.

    Evidence N-terminal protein sequencing and myeloma transfection/surface expression assay

    PMID:2269334

    Open questions at the time
    • Did not define the signaling function of the cytoplasmic tail
    • Stoichiometry and disulfide architecture unresolved
  2. 1992 High

    Showed CD79B and CD79A recruit distinct effectors and that their co-expression is sufficient for surface IgM, revealing functional non-redundancy within the heterodimer.

    Evidence Cytoplasmic tail pulldowns, PI3K association assay, and reconstitution in non-lymphoid AtT20 cells

    PMID:1373499 PMID:1439759

    Open questions at the time
    • Identity of associated 40/42-kDa phosphoproteins unresolved
    • How distinct effector recruitment translates to distinct outcomes not yet defined
  3. 1993 High

    Demonstrated through chimeras and transmembrane mutagenesis that CD79A and CD79B are necessary and sufficient for BCR signaling but engage different pathways, establishing the division of labor between the two ITAM-bearing chains.

    Evidence Chimeric receptor fusions, transmembrane mutagenesis, Ca2+ flux, phosphorylation, and co-IP of complex components

    PMID:7681402 PMID:7688784 PMID:8245014 PMID:8268137

    Open questions at the time
    • Molecular basis for the weaker tyrosine kinase activation through Ig-beta not defined
    • Did not identify the kinase activated by Ig-beta
  4. 1994 High

    Mapped the ITAM determinants of CD79B signaling, showing conserved residues are required and that BCR and TCR signaling subunits are functionally homologous.

    Evidence CD8/Ig-beta chimeras in T cell hybridomas with alanine-scan ITAM mutagenesis and IL-2/Ca2+ readouts

    PMID:8175787 PMID:8289790

    Open questions at the time
    • Did not connect specific ITAM residues to specific downstream effectors
  5. 1995 High

    Defined the biochemical mechanism by which phospho-CD79B ITAM activates Syk and showed CD79B is the dominant Syk ligand, explaining how the receptor couples to proximal kinase activation.

    Evidence In vitro kinase assays with ITAM phosphopeptides, tandem SH2 binding, and ITAM tyrosine mutagenesis

    PMID:7538118 PMID:8580068

    Open questions at the time
    • Did not address Syk activation kinetics in vivo
    • Other ITAM-binding partners not surveyed
  6. 1995 High

    Established that CD79B ITAM tyrosines transduce antigen-independent developmental signals driving the pre-B transition and allelic exclusion, distinguishing developmental from activation signaling.

    Evidence Transgenic mice expressing the Ig-beta cytoplasmic domain with tyrosine mutants and B cell developmental analysis

    PMID:7716544

    Open questions at the time
    • Downstream developmental effectors not identified at this stage
  7. 1995 Medium

    Showed CD79B determines antigen trafficking destination, linking receptor composition to antigen presentation kinetics.

    Evidence Fc receptor chimera expression with antigen presentation assays and endosomal compartment imaging

    PMID:7552998

    Open questions at the time
    • Single-lab chimeric approach
    • Molecular sorting signal in CD79B not yet mapped
  8. 1996 High

    Genetic knockout revealed an early, pre-BCR requirement for CD79B in productive V(D)J recombination, placing it upstream of immunoglobulin gene assembly.

    Evidence Ig-beta knockout mouse with flow cytometry and V(D)J recombination molecular assays

    PMID:8602530

    Open questions at the time
    • Mechanism linking Ig-beta to VH-to-DJH recombination not resolved
  9. 1996 Medium

    Identified intra- and extra-ITAM sequence determinants that tune CD79B signaling capacity relative to CD79A.

    Evidence FcgammaRII chimeric receptors with mutagenesis of QTAT and flanking sequences, multiple signaling readouts

    PMID:8798606

    Open questions at the time
    • Single lab
    • Structural basis for sequence-dependent kinase association not defined
  10. 1997 High

    Defined the CD79B-initiated signaling cascade in pro-B cells and showed CD79B engagement alone drives early developmental progression in vivo.

    Evidence Anti-Ig-beta crosslinking of primary pro-B cells, in vivo mAb treatment of RAG-2-deficient mice, phosphorylation profiling

    PMID:9354476

    Open questions at the time
    • Selectivity for ERK over JNK/p38 mechanistically unexplained
  11. 1997 High

    Showed the CD79A and CD79B cytoplasmic domains are independently sufficient for key developmental functions in vivo, and that heterodimer cooperativity is required for BCR-induced apoptosis.

    Evidence Transgenic IgM chimeric receptor mice with ITAM mutagenesis; chimeric dimer aggregation apoptosis system

    PMID:9057631 PMID:9151700

    Open questions at the time
    • Apoptosis cooperativity mechanism (idx 16) shown in a single lab
    • How redundancy is balanced in normal cells unresolved
  12. 1999 Medium

    Revealed that antigen induces dissociation of the Ig-alpha/Ig-beta module from mIg, providing a mechanism for receptor desensitization and for coupling signaling to antigen endocytosis.

    Evidence Co-IP after antigen stimulation with signaling assays and pharmacologic inhibitors; sucrose gradient and imaging (later work)

    PMID:10072076 PMID:10352267

    Open questions at the time
    • Single-lab co-IP-based destabilization model
    • Requirement of both chains for MIIC trafficking shown in single lab
  13. 2000 High

    Demonstrated that CLL-derived CD79B mutations directly impair BCR assembly and signal transduction, linking receptor defects to disease biology.

    Evidence Vaccinia recombinant expression in Jurkat cells, co-IP, MAPK activation assays with defined mutants

    PMID:10792036

    Open questions at the time
    • Single lap reconstitution system
    • Did not establish causal role in CLL pathogenesis in vivo
  14. 2001 High

    Genetic epistasis established that CD79B cytoplasmic signaling is essential when CD79A ITAM signaling is absent and placed BTK downstream of CD79B in development.

    Evidence Knock-in mice with ITAM/truncation mutations; RAG2/BTK double-knockout pro-B cell crosslinking with kinase Western blots

    PMID:11282988 PMID:11514602

    Open questions at the time
    • The BTK-dependent branch downstream of ERK/PLCgamma2 not molecularly defined
  15. 2002 High

    Characterized the exon-3-deleted CD79B splice variant as a dominant-negative regulator that down-modulates surface BCR and inhibits apoptosis in CLL, and explained CD79B-specific expression in plasma cells via Bob1/octamer control.

    Evidence Transfection of deltaCD79b into Burkitt lines with apoptosis/surface IgM assays and co-IP; promoter-reporter octamer-swap mutagenesis

    PMID:11907094 PMID:12115635 PMID:12384401

    Open questions at the time
    • Mechanism of ITAM-dependent apoptosis inhibition by deltaCD79b not fully resolved
    • Splicing regulation in vivo not addressed
  16. 2002 Medium

    Localized Ig-beta-specific PI3K activity to endocytic compartments and showed it is required for antigen-processing compartment formation rather than internalization.

    Evidence PI3K inhibitor treatment, antigen presentation assays, fluorescent lipid probes, electron microscopy

    PMID:12459553

    Open questions at the time
    • Single lab
    • Direct CD79B-PI3K recruitment mechanism in endosomes not defined
  17. 2006 High

    Defined the intermolecular disulfide (Ig-alpha C113-Ig-beta C135) and showed CD79B ITAM tyrosines set the BCR signaling threshold through control of receptor internalization.

    Evidence S2 cell reconstitution with cysteine mutagenesis; Igbeta(AA) ITAM knock-in mice with internalization, Ca2+, and kinase assays

    PMID:16818674 PMID:16877534

    Open questions at the time
    • How reduced internalization paradoxically prolongs signaling not fully mechanistically resolved
  18. 2007 High

    Identified Itch-dependent diubiquitinylation of CD79B as the signal directing endosomal sorting and antigen presentation, separable from internalization, and established CD79B loss-of-function as a cause of human agammaglobulinemia.

    Evidence Itch-/- B cells and ubiquitin-defective mutants with trafficking/presentation assays; human nonsense and G137S mutations with S2/293T reconstitution and patient analysis

    PMID:17675462 PMID:17709424 PMID:17878339

    Open questions at the time
    • Ubiquitin-reader machinery for endosomal sorting not identified
    • G137S characterization (idx 31) single cell-line study
  19. 2011 High

    Showed that ITAM monophosphorylation of CD79B engages an inhibitory SHIP-1/Dok-1 circuit required to maintain B cell anergy, distinguishing tolerogenic from activating signaling output.

    Evidence B cell-specific SHIP-1 conditional knockout with phosphoprotein analysis, signaling assays, and autoantibody measurement

    PMID:22078222

    Open questions at the time
    • Determinants biasing ITAM toward mono- vs. di-phosphorylation not defined
  20. 2013 Medium

    Revealed post-transcriptional control of CD79B abundance by IL-4/STAT6, identifying CD79B protein level as a tunable amplifier of BCR signaling.

    Evidence Primary B cell IL-4 culture, Western blot, co-IP, in vivo anti-IL-4 neutralization, ERK phosphorylation

    PMID:23776171

    Open questions at the time
    • Single lab
    • Mechanism of the mRNA-to-protein translational/stability gate not defined
  21. 2017 High

    Dissected the cooperative oncogenic mechanism showing CD79B and MYD88 mutations together block peripheral deletion and drive plasmablast differentiation, neither sufficient alone.

    Evidence Retroviral gene transfer into primary mouse B cells with in vivo chronic antigen stimulation and IgM glycosylation imaging

    PMID:28701369

    Open questions at the time
    • Molecular basis of CD79B-MYD88 synergy at the signaling level not fully mapped
  22. 2015 Medium

    Established CD79B Y196 ITAM mutations as a hotspot in immune-privileged-site lymphomas that, with MYD88 mutations, activate NF-kB, and showed CD79B overexpression drives ibrutinib resistance.

    Evidence Cohort sequencing of NF-kB pathway genes in PCNSL; cDNA overexpression/shRNA with AKT/MAPK readouts and inhibitor combinations

    PMID:26111727 PMID:26699656

    Open questions at the time
    • NF-kB activation in PCNSL is inferred, not directly assayed in idx 37
    • Resistance mechanism studied in single lab
  23. 2018 High

    Showed CD79B is required for lymphoma cell fitness and can act as an autonomous CD19-associated, ITAM/PI3K signaling module independent of other BCR components.

    Evidence CRISPR/Cas9 knockout, competitive growth assays, proximity ligation with CD19, ITAM mutagenesis, PI3K signaling assays

    PMID:29669863

    Open questions at the time
    • Physical basis of CD79B-CD19 proximity not structurally defined
  24. 2022 High

    Pinpointed CD79B as required for N-glycan maturation and ER exit of the BCR, with G137S unable to rescue, consolidating the assembly/trafficking checkpoint role.

    Evidence CRISPR/Cas9 knockout in human B lymphoma lines, endoglycosidase H assay, and rescue with wild-type vs. G137S CD79B

    PMID:36426942

    Open questions at the time
    • ER quality-control machinery acting on CD79B not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CD79B ITAM phosphorylation state, ubiquitin marks, and receptor trafficking are integrated to switch between tolerogenic, activating, and oncogenic outputs remains incompletely defined.
  • No unified model linking mono/di-ITAM phosphorylation to effector choice
  • Structural basis of CD79B-CD19 alternative module unknown
  • Mechanism of CD79B/MYD88 NF-kB synergy not resolved at molecular detail

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 3 GO:0060089 molecular transducer activity 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005768 endosome 3 GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3
Partners
BTKCD19CD79AITCHMYD88PIK3SYK
Complex memberships
B cell antigen receptor (BCR)

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1990 CD79B (Ig-beta/B29) was identified as a component of the IgM B cell antigen receptor complex by N-terminal amino acid sequencing, establishing that the B29 gene product forms a heterodimer with Ig-alpha (mb-1) and is required for surface IgM expression in myeloma transfection experiments. N-terminal protein sequencing, transfection/surface expression assay European journal of immunology High 2269334
1992 The cytoplasmic tail of CD79B (Ig-beta) associates with PI-3 kinase and unidentified 40- and 42-kDa phosphoproteins, but not with Src-family kinases Lyn or Fyn (which bind Ig-alpha), demonstrating that CD79B and CD79A recruit distinct cytoplasmic effectors through a shared 26-amino acid ITAM-containing motif. Cytoplasmic tail binding/pulldown assay, phosphoprotein association Science (New York, N.Y.) High 1439759
1992 Co-expression of MB-1 (Ig-alpha) and Ig-beta, but not MB-1 alone, is sufficient to promote high-level surface expression of mIgM in a non-lymphoid cell line (AtT20), and the reconstituted receptor mediates tyrosine phosphorylation of MB-1 and Ig-beta and increases PI3K activity upon crosslinking. Transfection into non-lymphoid cell line, anti-phosphotyrosine immunoblot, PI3K activity assay Proceedings of the National Academy of Sciences of the United States of America High 1373499
1993 Specific mutations in the IgM transmembrane domain that abolish Ca2+ flux and phosphorylation also uncouple mIg from Ig-alpha/Ig-beta; fusion of the Ig-beta cytoplasmic domain to inactive Ig reconstitutes Ca2+ responses only, while Ig-alpha fusion fully reconstitutes both Ca2+ and phosphorylation, demonstrating that Ig-alpha and Ig-beta are necessary and sufficient for BCR signal transduction but activate different signaling pathways. Transmembrane domain mutagenesis, chimeric receptor fusion, Ca2+ flux assay, phosphorylation assay The Journal of experimental medicine High 7688784
1993 CD8/Ig-beta chimeric receptors transduce signals (Ca2+ increase, MAP kinase phosphorylation) in B lymphoma cells upon crosslinking, but protein tyrosine kinase activation is only marginal via CD8/Ig-beta compared to CD8/Ig-alpha, providing first direct evidence that Ig-beta cytoplasmic tail has signaling capacity distinct from Ig-alpha. Chimeric receptor expression, anti-CD8 antibody crosslinking, intracellular Ca2+ measurement, MAP kinase phosphorylation assay European journal of immunology High 7681402
1993 Signaling-defective mutants of mIgM fail to associate with Ig-alpha and Ig-beta, demonstrating complete concordance between the IgM transmembrane region's ability to bind accessory molecules and its ability to transduce signals. Co-immunoprecipitation of BCR complex components in signaling vs. non-signaling mIgM mutants The Journal of biological chemistry High 8245014
1993 Cross-linkage of Ig-beta on human B cells activates tyrosine kinases, hydrolyzes phosphatidylinositides, and elevates intracellular Ca2+, demonstrating that Ig-beta ligation alone initiates BCR signal transduction pathways. Anti-Ig-beta mAb crosslinking, tyrosine kinase activation assay, phosphatidylinositide hydrolysis, intracellular Ca2+ measurement International immunology Medium 8268137
1994 Ig-beta cytoplasmic domain activates Ca2+ flux, IL-2 secretion, and protein tyrosine phosphorylation equivalent to TCR signaling when expressed as a chimeric CD8/Ig-beta receptor in T cells; conserved leucine (but not isoleucine) in the ITAM motif of Ig-beta is required for signaling, demonstrating functional homology between BCR and TCR signaling subunits. Chimeric receptor expression in T cell hybridoma, alanine substitution mutagenesis, Ca2+ flux, IL-2 ELISA, phosphotyrosine blot Molecular and cellular biology / The Journal of biological chemistry High 8175787 8289790
1995 Tyrosine-phosphorylated Ig-beta ITAM peptides stimulate Syk kinase activity up to 10-fold in vitro; maximal activation requires both Syk SH2 domains and phosphorylation of both ITAM tyrosines; mechanism involves Syk autophosphorylation, establishing that phospho-Ig-beta ITAM binding to Syk tandem SH2 domains activates Syk by autophosphorylation. In vitro kinase assay with phosphopeptides, SH2 domain binding assay, mutagenesis of ITAM tyrosines The Journal of biological chemistry High 7538118
1995 The cytoplasmic domain of Ig-beta is sufficient to induce the pre-B cell transition and allelic exclusion in transgenic mice; these functions require conserved tyrosine residues in the Ig-beta cytoplasmic tail, establishing that Ig-beta ITAM tyrosines mediate antigen-independent developmental signaling. Transgenic mouse model, tyrosine mutants, B cell developmental analysis Science (New York, N.Y.) High 7716544
1995 Tyrosine-phosphorylated Ig-beta is a major ligand for the tandem SH2 domains of Syk in activated B cells, with binding occurring predominantly via Ig-beta rather than Ig-alpha, indicating these two receptor components couple to distinct signaling pathways. In vitro SH2 domain binding assay, identification of phosphoproteins from activated B cell lysates International immunology Medium 8580068
1995 Ig-beta targets antigen to transferrin receptor-containing recycling endosomes (minor MHC class II population), distinct from Ig-alpha which targets to MHC class II-rich compartments (MIIC), demonstrating that the composition of BCR determines antigen trafficking and presentation kinetics. Fc receptor chimera expression, antigen presentation assay, endosomal compartment analysis by fluorescence microscopy Immunity Medium 7552998
1996 Mice lacking Ig-beta have a complete block in B cell development at the immature CD43+B220+ stage; VH-to-DJH recombination and IgH mRNA expression are compromised, revealing an early, pre-BCR requirement for Ig-beta in productive V(D)J recombination. Ig-beta knockout mouse, flow cytometry, Southern blot/PCR for V(D)J recombination Science (New York, N.Y.) High 8602530
1996 The signaling capacity of the Ig-beta ITAM is regulated by peptide sequences inside the ITAM (QTAT region before the second conserved tyrosine) and by flanking sequences outside the ITAM; the QTAT vs. DCSM difference between Ig-beta and Ig-alpha determines in vitro Fyn kinase association and in vivo signaling capability. FcgammaRII chimeric receptor expression in B cells, cytokine secretion, Ca2+ flux, tyrosine kinase activation assay The Journal of biological chemistry Medium 8798606
1997 Cross-linking of Ig-beta on mu-negative pro-B cells induces tyrosine phosphorylation of Ig-alpha, Syk, PI3K, Vav, SLP-76, and MAP kinase ERK (but not JNK/SAPK or p38); anti-Ig-beta treatment of RAG-2-deficient mice induces pro-B to small pre-B cell differentiation, demonstrating that Ig-beta signals are sufficient to drive early B cell developmental progression. Anti-Ig-beta crosslinking on primary pro-B cells, in vivo mAb treatment of RAG-2-deficient mice, phosphorylation assays, flow cytometry Immunity High 9354476
1997 Ig-alpha and Ig-beta cytoplasmic domains are independently sufficient to mediate allelic exclusion, rescue B cell development in Ig-mu-deficient mice, and signal B7 upregulation as IgM chimeric transgenic receptors; an IgM/beta with mutant ITAM fails these functions, confirming ITAM dependence. Transgenic mouse lines with IgM/Ig-beta chimeric receptors, ITAM tyrosine mutagenesis, flow cytometry of B cell subsets The Journal of experimental medicine High 9151700
1997 Heterodimers of Ig-alpha and Ig-beta together efficiently induce apoptosis in WEHI-231 cells upon aggregation, while homodimers of either chain do not; apoptosis is associated with Syk tyrosine phosphorylation, demonstrating that heterodimer cooperativity between Ig-alpha and Ig-beta is required for BCR-induced apoptosis. Chimeric dimer aggregation system, apoptosis assay, phosphotyrosine blot for Syk Blood Medium 9057631
1999 Antigen stimulation leads to dissociation of Ig-alpha/Ig-beta from mIg (BCR destabilization), temporally correlated with receptor desensitization; destabilization requires tyrosine kinase activation, is not induced by phosphatase inhibitors, and 'dissociated' Ig-alpha/Ig-beta complexes remain responsive to anti-Ig-beta stimulation, indicating mIg-transducer uncoupling as a mechanism of BCR desensitization. Co-immunoprecipitation after antigen stimulation, signaling assays, pharmacologic inhibitors Immunity Medium 10072076
1999 Both Ig-alpha and Ig-beta are required for BCR trafficking to MHC class II-enriched compartments (MIIC) and enhanced antigen presentation at low antigen concentrations; neither chain alone is sufficient; ITAM tyrosines of Ig-alpha are required for MIIC access. Chimeric receptor expression, antigen presentation assay, fluorescence microscopy for MIIC Journal of immunology (Baltimore, Md. : 1950) Medium 10352267
1999 An alternatively spliced CD79B transcript lacking exon 3 (encoding the extracellular Ig-like domain) is increased in CLL B cells and in normal activated B cells; this variant is detectable as protein; its relative expression is significantly higher in CLL vs. normal B cells, suggesting alternative splicing as a mechanism for reduced BCR surface expression in CLL. RT-PCR, radioactive PCR quantification, direct sequencing, SSCP analysis Blood Medium 10090943
2000 CLL-derived CD79B mutants have defined functional defects: a truncation in the transmembrane domain prevents association with mu and mb-1 at the cell surface; a mutant lacking the C-terminal ITAM tyrosine and distal residues reaches the cell surface but shows significantly impaired MAPK signaling after anti-IgM stimulation, demonstrating that CLL CD79B mutations directly impair BCR assembly and signal transduction. Vaccinia virus recombinant expression in Jurkat T cells, co-immunoprecipitation, MAPK activation assay Proceedings of the National Academy of Sciences of the United States of America High 10792036
2001 Ig-alpha ITAM tyrosine mutation combined with Ig-beta cytoplasmic tail truncation completely blocks B cell development at the pro-B stage, while Ig-alpha ITAM mutation alone only partially impairs B cell subsets, demonstrating that Ig-beta cytoplasmic domain is essential when Ig-alpha ITAM signaling is absent and revealing functional redundancy with Ig-alpha in B cell development. Gene targeting (knock-in mice with phenylalanine substitutions and Ig-beta truncation), flow cytometry The Journal of experimental medicine High 11514602
2001 Bruton's tyrosine kinase (BTK) is required for CD79b-mediated pro-B to pre-B cell transition: BTK is phosphorylated upon CD79b crosslinking; RAG2/BTK double-KO pro-B cells fail to differentiate after CD79b crosslinking despite normal ERK and PLCgamma2 phosphorylation, placing BTK downstream of CD79b but in a pathway separate from Erk/PLCgamma2. RAG2/BTK double-knockout mouse, CD79b crosslinking, Western blot for BTK phosphorylation and downstream kinases International immunology High 11282988
2002 The alternatively spliced CD79B variant (DeltaCD79b, lacking exon 3) is overexpressed in CLL and inhibits BCR-mediated apoptosis; when transfected into Ramos-EHRB cells it converts them from sensitive to resistant to anti-Fcmu-induced apoptosis; inhibitory activity requires intact leader sequence (for ER trafficking) and a functional ITAM in its cytoplasmic tail; overexpression does not reduce cell-surface BCR levels. Transfection of DeltaCD79b into Burkitt lymphoma cell lines, apoptosis assay, flow cytometry Blood High 12384401
2002 Alternatively spliced deltaCD79b protein fails to form heterodimers with full-length Ig-beta, does not mediate IgM transport to the cell surface, and when overexpressed competes with full-length Ig-alpha/Ig-beta to down-modulate surface IgM and cause ER retention, revealing a dominant-negative mechanism for BCR downregulation. Transfection in 293T cells, co-immunoprecipitation, surface IgM flow cytometry, ER retention assay European journal of immunology Medium 12115635
2002 Igbeta, but not Igalpha, activates PI3K in endocytic compartments; PI3K inhibitors block Igbeta-mediated de novo formation of multivesicular antigen-processing compartments and antigen presentation, but do not block antigen internalization or degradation, placing Igbeta-PI3K signaling specifically at the endosomal sorting step required for antigen presentation. PI3K inhibitor treatment, antigen presentation assay, fluorescent PI3K lipid probes in endocytic compartments, electron microscopy The Journal of biological chemistry Medium 12459553
2005 Antigen stimulation physically separates Ig-alpha/Ig-beta from mu heavy chain; after separation, Ig-alpha/Ig-beta localizes to GM1-containing lipid microdomains while unsheathed mu heavy chain colocalizes with clathrin-coated vesicles; preventing receptor destabilization blocks mu association with clathrin vesicles, demonstrating that BCR dissociation enables concomitant signaling (through Ig-alpha/Ig-beta in rafts) and antigen delivery (through mIg via clathrin endocytosis). Sucrose gradient fractionation, confocal and electron microscopy, clathrin colocalization assay Journal of immunology (Baltimore, Md. : 1950) Medium 15972641
2006 Cysteines 113 of Ig-alpha and 135 of Ig-beta form the intermolecular disulfide bond stabilizing the Ig-alpha/Ig-beta heterodimer; Ig-beta contains additional intramolecular disulfide bonds (C65-C120 canonical Ig fold; C43-C124); Ig-alpha C113S mutation reduces mIgM surface expression in B cells, indicating the intermolecular disulfide is required for efficient BCR assembly. Drosophila S2 cell reconstitution, cysteine-to-serine mutagenesis, non-reducing SDS-PAGE, surface IgM flow cytometry International immunology High 16877534
2006 Ig-beta ITAM tyrosine residues are required for steady-state and ligand-mediated BCR internalization in mature B cells in vivo; Igbeta(AA) knock-in mice show decreased BCR internalization, higher surface IgM/IgD, decreased Src and Syk activation but paradoxically enhanced and prolonged BCR signaling (Ca2+ flux, AKT, ERK), and enhanced T-independent antigen response, establishing that Ig-beta ITAM tyrosines set BCR signaling threshold by regulating receptor internalization. Gene targeting (Igbeta ITAM tyrosine-to-alanine knock-in), BCR internalization assay, flow cytometry, Ca2+ flux, Western blot for kinase activation The Journal of experimental medicine High 16818674
2007 Ig-beta is diubiquitinylated in a process dependent on the E3 ligase Itch; Itch-/- B cells show defective ligand-induced BCR internalization and failure to traffic to late endosomal antigen-processing compartments; ubiquitin attachment to Ig-beta is dispensable for internalization but required for endosomal sorting and antigen presentation to T cells. Itch-/- B lymphocytes, ubiquitinylation-defective receptor mutants, BCR internalization assay, antigen presentation assay, endocytic trafficking by confocal microscopy Journal of immunology (Baltimore, Md. : 1950) High 17878339
2007 A homozygous nonsense mutation in Igbeta causes agammaglobulinemia in a human patient with a complete block at the pro-B to pre-B transition; transfection in Drosophila S2 cells shows the mutant Igbeta can no longer associate with Igalpha and BCR complex assembly on the cell surface is abrogated. Patient bone marrow immunofluorescence, Drosophila S2 cell transfection/co-IP, sequencing The Journal of experimental medicine High 17709424
2007 A hypomorphic Igbeta G137S mutation (adjacent to the cysteine required for Igalpha-Igbeta disulfide bond) in a patient with immunodeficiency results in inefficient disulfide-linked complex formation and reduced mIgM surface expression; this minor inefficiency in BCR surface delivery profoundly impairs B cell development. Expression vectors in 293T and Jurkat cells, co-IP, surface IgM flow cytometry, patient B cell analysis Journal of immunology (Baltimore, Md. : 1950) Medium 17675462
2011 In anergic B cells, biased BCR ITAM monophosphorylation (on both CD79A and CD79B ITAMs) constitutively activates SHIP-1 and its adaptor Dok-1; B cell-specific SHIP-1 deletion restores BCR signaling and breaks anergy, demonstrating that partial (mono)phosphorylation of CD79B ITAM engages an inhibitory SHIP-1/Dok-1 circuit required to maintain B cell anergy. B cell-specific SHIP-1 knockout, phosphoprotein analysis, BCR signaling assays, autoantibody measurement, flow cytometry for anergic phenotype Immunity High 22078222
2013 IL-4 markedly upregulates Ig-beta protein expression (requiring STAT6) in primary B cells that otherwise have abundant mRNA but little protein; elevated Ig-beta forms heterodimers with Ig-alpha, promotes IgM maturation and surface expression, and amplifies BCR signaling in a Lyn-dependent manner in vitro and in vivo. Primary B cell culture with IL-4, Western blot, co-IP, surface IgM flow cytometry, in vivo anti-IL-4 neutralization, ERK phosphorylation assay Journal of immunology (Baltimore, Md. : 1950) Medium 23776171
2017 CD79B mutations alone increase surface IgM but do not enhance B cell survival, proliferation, or NF-kB markers; MYD88 mutation decreases surface IgM via intracellular retention; CD79B mutation counteracts MYD88-mediated IgM intracellular retention; in B cells chronically stimulated by self-antigen, combined CD79B and MYD88 mutations block peripheral deletion and trigger plasmablast differentiation, while each mutation alone does not—revealing synergistic cooperation requiring both mutations. Retroviral gene transfer into primary mouse B cells, flow cytometry, in vivo chronic antigen stimulation model, immunofluorescence for IgM glycosylation state The Journal of experimental medicine High 28701369
2018 CRISPR/Cas9 deletion of CD79B in Burkitt lymphoma (Ramos) cells impairs cell fitness and competitive growth; Ig-beta can be expressed on the B cell surface in the absence of other BCR components, where it is found in proximity to CD19 and signals in an ITAM-dependent manner, constituting an alternative signaling module with CD19 that supports B cell survival via ITAM/PI3K signaling. CRISPR/Cas9 knockout, competitive growth assay, proximity ligation assay, ITAM mutagenesis, PI3K signaling assay The EMBO journal High 29669863
2022 CRISPR/Cas9 deletion of CD79B in human B lymphoma lines causes loss of surface IgM, a block in N-glycan maturation (accumulation of endoglycosidase H-sensitive immature proteins), and retention of BCR components in the ER; rescue with wild-type CD79B restores surface IgM with mature glycosylation, while the naturally occurring CD79B G137S mutant (which disrupts Igalpha/Igbeta heterodimerization) does not restore surface expression. CRISPR/Cas9 knockout in human B cell lines, endoglycosidase H assay, flow cytometry, rescue with wild-type or mutant CD79B Journal of immunology (Baltimore, Md. : 1950) High 36426942
2015 CD79B Y196 mutations in the ITAM domain are hallmark mutations of primary CNS DLBCL (found in up to 83% of cases); these mutations, together with MYD88 mutations, constitutively activate the NF-kB pathway in immune-privileged site lymphomas, substituting for the lack of antigen stimuli in the CNS. Systematic sequencing of 21 NF-kB pathway genes in 71 PCNSL cases, pyrosequencing validation in additional cohorts Neuropathology and applied neurobiology Medium 26111727
2015 CD79B overexpression in ABC-DLBCL is sufficient to induce resistance to ibrutinib and enhances AKT and MAPK activation; depletion of CD79B sensitizes resistant cells to ibrutinib and reduces AKT/MAPK phosphorylation; combination of AKT or MAPK inhibitors with ibrutinib circumvents CD79B-mediated resistance. cDNA microarray, Western blot, cDNA overexpression, shRNA knockdown, cell viability assay, kinase inhibitor combination Leukemia & lymphoma Medium 26699656
2002 Bob1 (OCA-B/OBF-1) transactivates the B29 (CD79b) promoter but not the mb-1 (CD79a) promoter; differential transactivation is determined solely by the octamer sequence: the B29 octamer (ATGCAAAT) supports Bob1 binding while the mb-1 octamer does not; octamer swapping transfers Bob1 responsiveness, explaining why CD79b (but not CD79a) is expressed in plasma cells. Promoter-reporter cotransfection, octamer swap mutagenesis, silencer mutagenesis Journal of immunology (Baltimore, Md. : 1950) Medium 11907094

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1992 The B cell antigen receptor complex: association of Ig-alpha and Ig-beta with distinct cytoplasmic effectors. Science (New York, N.Y.) 290 1439759
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 271 25925619
1995 Syk protein-tyrosine kinase is regulated by tyrosine-phosphorylated Ig alpha/Ig beta immunoreceptor tyrosine activation motif binding and autophosphorylation. The Journal of biological chemistry 240 7538118
2009 Therapeutic potential of an anti-CD79b antibody-drug conjugate, anti-CD79b-vc-MMAE, for the treatment of non-Hodgkin lymphoma. Blood 230 19633198
1996 Regulation of an early developmental checkpoint in the B cell pathway by Ig beta. Science (New York, N.Y.) 222 8602530
1993 Signal transduction by immunoglobulin is mediated through Ig alpha and Ig beta. The Journal of experimental medicine 205 7688784
2015 Recurrent mutations of CD79B and MYD88 are the hallmark of primary central nervous system lymphomas. Neuropathology and applied neurobiology 186 26111727
2013 High prevalence of oncogenic MYD88 and CD79B mutations in diffuse large B-cell lymphomas presenting at immune-privileged sites. Blood cancer journal 166 24013661
2011 Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy. Immunity 140 22078222
1993 Differential signaling through the Ig-alpha and Ig-beta components of the B cell antigen receptor. European journal of immunology 130 7681402
2015 Anti-CD22 and anti-CD79B antibody drug conjugates are active in different molecular diffuse large B-cell lymphoma subtypes. Leukemia 127 25708834
1990 Identification of the genes encoding the IgM-alpha and Ig-beta components of the IgM antigen receptor complex by amino-terminal sequencing. European journal of immunology 127 2269334
1995 The role of Ig beta in precursor B cell transition and allelic exclusion. Science (New York, N.Y.) 113 7716544
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
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
1995 Role of B cell receptor Ig alpha and Ig beta subunits in MHC class II-restricted antigen presentation. Immunity 89 7552998
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
1995 The cytoplasmic domains of immunoglobulin (Ig) alpha and Ig beta can independently induce the precursor B cell transition and allelic exclusion. The Journal of experimental medicine 76 7595209
2002 B cell progenitors are arrested in maturation but have intact VDJ recombination in the absence of Ig-alpha and Ig-beta. Journal of immunology (Baltimore, Md. : 1950) 75 12097390
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
1992 The membrane IgM-associated proteins MB-1 and Ig-beta are sufficient to promote surface expression of a partially functional B-cell antigen receptor in a nonlymphoid cell line. Proceedings of the National Academy of Sciences of the United States of America 68 1373499
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
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 66 38203179
1997 Aberrations of the B-cell receptor B29 (CD79b) gene in chronic lymphocytic leukemia. Blood 66 9269755
2018 Continuous signaling of CD79b and CD19 is required for the fitness of Burkitt lymphoma B cells. The EMBO journal 62 29669863
2007 Mutations of the Igbeta gene cause agammaglobulinemia in man. The Journal of experimental medicine 54 17709424
2007 Ubiquitinylation of Ig beta dictates the endocytic fate of the B cell antigen receptor. Journal of immunology (Baltimore, Md. : 1950) 54 17878339
1993 Signaling-defective mutants of the B lymphocyte antigen receptor fail to associate with Ig-alpha and Ig-beta/gamma. The Journal of biological chemistry 54 8245014
2016 Frequent MYD88 L265P and CD79B Mutations in Primary Breast Diffuse Large B-Cell Lymphoma. The American journal of surgical pathology 52 26752547
1994 Ig alpha and Ig beta are functionally homologous to the signaling proteins of the T-cell receptor. Molecular and cellular biology 51 8289790
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
2007 Cutting edge: a hypomorphic mutation in Igbeta (CD79b) in a patient with immunodeficiency and a leaky defect in B cell development. Journal of immunology (Baltimore, Md. : 1950) 48 17675462
2013 CD79B and MYD88 mutations in diffuse large B-cell lymphoma. Human pathology 47 24444466
2022 Mechanism of CD79A and CD79B Support for IgM+ B Cell Fitness through B Cell Receptor Surface Expression. Journal of immunology (Baltimore, Md. : 1950) 45 36426942
2020 Oncogenic Mutations of MYD88 and CD79B in Diffuse Large B-Cell Lymphoma and Implications for Clinical Practice. Cancers 43 33050534
2017 Frequency of MYD88 and CD79B mutations, and MGMT methylation in primary central nervous system diffuse large B-cell lymphoma. Neuropathology : official journal of the Japanese Society of Neuropathology 42 28856744
2009 In vivo effects of targeting CD79b with antibodies and antibody-drug conjugates. Molecular cancer therapeutics 42 19808977
1999 Ig alpha and Ig beta are required for efficient trafficking to late endosomes and to enhance antigen presentation. Journal of immunology (Baltimore, Md. : 1950) 41 10352267
2002 The alternative transcript of CD79b is overexpressed in B-CLL and inhibits signaling for apoptosis. Blood 40 12384401
2015 CD79B limits response of diffuse large B cell lymphoma to ibrutinib. Leukemia & lymphoma 39 26699656
2017 Synergistic cooperation and crosstalk between MYD88 and mutations that dysregulate CD79B and surface IgM. The Journal of experimental medicine 37 28701369
1995 Alternative splicing of CD79a (Ig-alpha/mb-1) and CD79b (Ig-beta/B29) RNA transcripts in human B cells. Molecular immunology 37 7643857
1997 Antigen endocytosis and presentation mediated by human membrane IgG1 in the absence of the Ig(alpha)/Ig(beta) dimer. The EMBO journal 35 9233794
1998 Physical linkage of the human growth hormone gene cluster and the CD79b (Ig beta/B29) gene. Genomics 33 9521881
1997 B-cell antigen receptor-induced apoptosis requires both Ig alpha and Ig beta. Blood 33 9057631
1994 The internalization of the IgG2a antigen receptor does not require the association with Ig-alpha and Ig-beta but the activation of protein tyrosine kinases does. European journal of immunology 33 8125135
2022 MYD88L265P and CD79B double mutations type (MCD type) of diffuse large B-cell lymphoma: mechanism, clinical characteristics, and targeted therapy. Therapeutic advances in hematology 32 35126963
1999 CD79b expression in B cell chronic lymphocytic leukemia: its implication for minimal residual disease detection. Leukemia 31 10516749
1994 Activation of B- and T-cells by the cytoplasmic domains of the B-cell antigen receptor proteins Ig-alpha and Ig-beta. The Journal of biological chemistry 31 8175787
2020 Polatuzumab vedotin: an investigational anti-CD79b antibody drug conjugate for the treatment of diffuse large B-cell lymphoma. Expert opinion on investigational drugs 30 32700972
2013 IL-4 upregulates Igα and Igβ protein, resulting in augmented IgM maturation and B cell receptor-triggered B cell activation. Journal of immunology (Baltimore, Md. : 1950) 30 23776171
2000 Usefulness of CD79b expression in the diagnosis of B-cell chronic lymphoproliferative disorders. American journal of clinical pathology 30 10874881
2017 Patients with primary breast and primary female genital tract diffuse large B cell lymphoma have a high frequency of MYD88 and CD79B mutations. Annals of hematology 29 28803429
2005 Independent trafficking of Ig-alpha/Ig-beta and mu-heavy chain is facilitated by dissociation of the B cell antigen receptor complex. Journal of immunology (Baltimore, Md. : 1950) 29 15972641
2003 CD79b expression in chronic lymphocytic leukemia. Association with trisomy 12 and atypical immunophenotype. Archives of pathology & laboratory medicine 28 12708898
1995 Tyrosine-phosphorylated forms of Ig beta, CD22, TCR zeta and HOSS are major ligands for tandem SH2 domains of Syk. International immunology 28 8580068
2019 Evaluation and use of an anti-cynomolgus monkey CD79b surrogate antibody-drug conjugate to enable clinical development of polatuzumab vedotin. British journal of pharmacology 27 31270798
1998 Cross-lineage expression of Ig-beta (B29) in thymocytes: positive and negative gene regulation to establish T cell identity. Proceedings of the National Academy of Sciences of the United States of America 27 9618498
1996 Regulation of ITAM signaling by specific sequences in Ig-beta B cell antigen receptor subunit. The Journal of biological chemistry 27 8798606
1999 Analysis of the B-cell receptor B29 (CD79b) gene in familial chronic lymphocytic leukemia. Blood 26 10552962
1993 The human Ig-beta cDNA sequence, a homologue of murine B29, is identical in B cell and plasma cell lines producing all the human Ig isotypes. Journal of immunology (Baltimore, Md. : 1950) 26 8419481
2017 Anti-CD22 and anti-CD79b antibody-drug conjugates preferentially target proliferating B cells. British journal of pharmacology 25 28009435
2000 Aberrant B cell receptor signaling from B29 (Igbeta, CD79b) gene mutations of chronic lymphocytic leukemia B cells. Proceedings of the National Academy of Sciences of the United States of America 25 10792036
2013 CD79B and MYD88 Mutations in Splenic Marginal Zone Lymphoma. ISRN oncology 24 23378931
2004 Basal Igalpha/Igbeta signals trigger the coordinated initiation of pre-B cell antigen receptor-dependent processes. Journal of immunology (Baltimore, Md. : 1950) 24 15240688
1994 The complete sequence of the human CD79b (Ig beta/B29) gene: identification of a conserved exon/intron organization, immunoglobulin-like regulatory regions, and allelic polymorphism. Immunogenetics 24 7913081
2022 Anti-CD79B Antibody-Drug Conjugate DCDS0780A in Patients with B-Cell Non-Hodgkin Lymphoma: Phase 1 Dose-Escalation Study. Clinical cancer research : an official journal of the American Association for Cancer Research 23 34980599
2016 MYD88, CD79B, and CARD11 gene mutations in CD5-positive diffuse large B-cell lymphoma. Cancer 23 27915469
2014 B-cell inhibition by cross-linking CD79b is superior to B-cell depletion with anti-CD20 antibodies in treating murine collagen-induced arthritis. European journal of immunology 23 25471597
2001 Bruton's tyrosine kinase is required for signaling the CD79b-mediated pro-B to pre-B cell transition. International immunology 22 11282988
2006 Identification of disulfide bonds in the Ig-alpha/Ig-beta component of the B cell antigen receptor using the Drosophila S2 cell reconstitution system. International immunology 21 16877534
2006 Analysis of the individual contributions of Igalpha (CD79a)- and Igbeta (CD79b)-mediated tonic signaling for bone marrow B cell development and peripheral B cell maturation. Journal of immunology (Baltimore, Md. : 1950) 21 17114463
2004 The avian B-cell receptor complex: distinct roles of Igalpha and Igbeta in B-cell development. Immunological reviews 21 14962183
1996 Differential expression of B29 (CD79b) and mb-1 (CD79a) proteins in acute lymphoblastic leukaemia. Leukemia 21 8656670
2020 Targeting CD79b for Chimeric Antigen Receptor T-Cell Therapy of B-Cell Lymphomas. Targeted oncology 20 32495161
2014 Therapeutic targeting of the BCR-associated protein CD79b in a TCR-based approach is hampered by aberrant expression of CD79b. Blood 20 25414443
1993 Signal transduction in human B cells initiated via Ig beta ligation. International immunology 19 8268137
1993 Isolation and chromosomal mapping of the human immunoglobulin-associated B29 gene (IGB). Genomics 19 8486355
2013 EZH2 and CD79B mutational status over time in B-cell non-Hodgkin lymphomas detected by high-throughput sequencing using minimal samples. Cancer cytopathology 18 23361872
2002 Bob1 (OCA-B/OBF-1) differential transactivation of the B cell-specific B29 (Ig beta) and mb-1 (Ig alpha) promoters. Journal of immunology (Baltimore, Md. : 1950) 18 11907094
2002 Alternatively spliced forms of Igalpha and Igbeta prevent B cell receptor expression on the cell surface. European journal of immunology 18 12115635
2011 Downregulation of the B-cell receptor signaling component CD79b in plasma cell myeloma: a possible post transcriptional regulation. Pathology international 17 21355953
1996 Counterselection against D mu is mediated through immunoglobulin (Ig)alpha-Igbeta. The Journal of experimental medicine 17 8976164
2020 Morphologic Patterns and the Correlation With MYD88 L265P, CD79B Mutations in Primary Adrenal Diffuse Large B-Cell Lymphoma. The American journal of surgical pathology 16 31609782
2005 Ig-independent Ig beta expression on the surface of B lymphocytes after B cell receptor aggregation. Journal of immunology (Baltimore, Md. : 1950) 15 15661909
1999 Modifications of Igalpha and Igbeta expression as a function of B lineage differentiation. The Journal of biological chemistry 15 10383452
1997 Silencer elements controlling the B29 (Igbeta) promoter are neither promoter- nor cell-type-specific. Proceedings of the National Academy of Sciences of the United States of America 15 9356446
2024 A single-centre, real-world study of BTK inhibitors for the initial treatment of MYD88mut /CD79Bmut diffuse large B-cell lymphoma. Cancer medicine 14 38457222
2023 Chimeric antigen receptor T cells to target CD79b in B-cell lymphomas. Journal for immunotherapy of cancer 14 38007239
2005 Ig alpha/Ig beta complexes generate signals for B cell development independent of selective plasma membrane compartmentalization. Journal of immunology (Baltimore, Md. : 1950) 14 15661879
2020 Polatuzumab vedotin, an anti-CD79b antibody-drug conjugate for the treatment of relapsed/refractory diffuse large B-cell lymphoma. Future oncology (London, England) 13 32954807
2002 Phosphoinositide 3-kinase activation by Igbeta controls de novo formation of an antigen-processing compartment. The Journal of biological chemistry 13 12459553
2001 Multitasking of Ig-alpha and Ig-beta to regulate B cell antigen receptor function. International reviews of immunology 13 11913945
1999 Widespread B29 (CD79b) gene defects and loss of expression in chronic lymphocytic leukemia. Leukemia & lymphoma 13 10048429

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