Affinage

CD79A

B-cell antigen receptor complex-associated protein alpha chain · UniProt P11912

Round 2 corrected
Length
226 aa
Mass
25.0 kDa
Annotated
2026-04-28
130 papers in source corpus 27 papers cited in narrative 27 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD79A (Igα/mb-1) is a B-cell-lineage-restricted transmembrane glycoprotein that heterodimerizes with CD79B (Igβ) to form the obligate signaling subunit of the B-cell antigen receptor (BCR), associating with all five classes of membrane-bound immunoglobulin to transduce antigen-dependent and tonic signals essential for B-cell development and activation (PMID:1881434, PMID:9354476). Upon BCR engagement, Src-family kinases asymmetrically phosphorylate the Igα ITAM — predominantly at the N-terminal tyrosine — enabling dual-SH2-domain recruitment and activation of Syk, which in turn drives PLCγ2/Ca²⁺ mobilization, while a non-ITAM tyrosine (Y204) directly recruits the adaptor BLNK/SLP-65 to couple Syk to downstream NF-κB and MAPK pathways (PMID:9531288, PMID:11909947, PMID:7500027). Serine/threonine phosphorylation of the Igα cytoplasmic tail negatively regulates ITAM signaling amplitude, and truncation of this tail causes constitutive signaling and developmental arrest of transitional B cells (PMID:10900006, PMID:10591178). Homozygous loss-of-function mutations in CD79A cause human agammaglobulinemia with a complete block at the pro-B to pre-B transition, whereas gain-of-function ITAM mutations in ABC-DLBCL drive constitutive NF-κB activation (PMID:10525050, PMID:21324920).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1988 High

    Identification of mb-1 as a B-cell-specific surface glycoprotein gene resolved the question of which lineage-restricted transmembrane molecules might couple surface immunoglobulin to intracellular signaling.

    Evidence cDNA cloning with antibody staining of pre-B and mature B cell lines vs. T cells and fibroblasts

    PMID:2463161

    Open questions at the time
    • No signaling function yet demonstrated
    • Heterodimeric partner (Igβ) not yet identified in this study
  2. 1991 High

    Reconstitution of surface IgM expression in fibroblasts with only Igα and Igβ established that this heterodimer is the minimal signaling unit of the BCR and associates with all five immunoglobulin isotypes, resolving the composition of the BCR signaling module.

    Evidence Fibroblast reconstitution with co-immunoprecipitation across IgM/IgD/IgG/IgA/IgE

    PMID:1881434

    Open questions at the time
    • Kinase(s) responsible for signal initiation not yet identified
    • No structural data on Igα/Igβ heterodimer
  3. 1992 High

    Discovery that the tyrosine kinase Syk physically associates with Igα and is activated upon BCR cross-linking identified the first kinase in the Igα proximal signaling cascade, establishing a direct kinase–ITAM connection.

    Evidence Reciprocal co-immunoprecipitation, in vitro kinase assay, and peptide mapping in B cell lines

    PMID:1569106

    Open questions at the time
    • Which ITAM tyrosines are required for Syk binding not yet resolved
    • Downstream substrates of Syk in this context unknown
  4. 1995 High

    Demonstration that both Syk SH2 domains are required for ITAM binding and that ITAM recruitment precedes Syk autophosphorylation and Ca²⁺ mobilization established the ordered activation mechanism of BCR proximal signaling, while parallel work showed SHP-1 constitutively associates with resting BCR to restrain Igα phosphorylation.

    Evidence Syk-knockout B cells reconstituted with SH2/kinase mutants; SHP-1 co-IP with phosphatase activity assays in motheaten mice

    PMID:7500027 PMID:7539038

    Open questions at the time
    • Structural basis of dual SH2–ITAM engagement not resolved
    • Identity of kinase initially phosphorylating the ITAM not established
  5. 1997 High

    Finding that the Igα/Igβ heterodimer is expressed on pro-B cells before μ heavy chain and can signal through Syk/PI3K/Vav to drive differentiation revealed that Igα has signaling functions independent of complete BCR assembly.

    Evidence Anti-Igβ cross-linking on RAG-2-deficient pro-B cells with phosphorylation cascade analysis and in vivo differentiation

    PMID:9354476

    Open questions at the time
    • Whether Igα or Igβ tail is the dominant contributor to these pre-BCR-independent signals not resolved
  6. 1998 High

    Systematic ITAM tyrosine mutagenesis revealed that phosphorylation of the Igα ITAM is asymmetric, with the N-terminal tyrosine (YEGL) accounting for >80% of phosphorylation and being sufficient for most downstream signaling except full Syk activation, which requires both tyrosines.

    Evidence MHC class II chimeric receptor system with Y→F point mutations, phosphorylation assays, Ca²⁺ mobilization

    PMID:9531288

    Open questions at the time
    • Structural explanation for asymmetric phosphorylation unknown
    • Kinase selectivity for N- vs. C-terminal ITAM tyrosine not identified
  7. 1999 High

    A human homozygous CD79A splice mutation causing complete B-cell developmental arrest at the pro-B/pre-B transition established CD79A as a causative gene for agammaglobulinemia, while truncation of the Igα cytoplasmic tail in mice paradoxically caused constitutive BCR signaling and loss of transitional B cells, revealing a dual role as both activator and negative regulator.

    Evidence Human patient genetics with bone marrow staging; mb-1Δc/Δc knock-in mice with flow cytometric B-cell profiling

    PMID:10525050 PMID:10591178

    Open questions at the time
    • Mechanism by which tail truncation causes constitutive signaling not molecularly defined
    • Additional human CD79A mutations not yet cataloged
  8. 2000 High

    Mutation of all serine/threonine residues in the Igα tail to alanine/valine augmented ITAM tyrosine phosphorylation, identifying Ser/Thr phosphorylation as a dedicated negative-feedback mechanism that attenuates BCR signal amplitude.

    Evidence Comprehensive S/T→A/V mutagenesis in single-chain Fv/Igα chimera and full BCR, tyrosine phosphorylation readout

    PMID:10900006

    Open questions at the time
    • Identity of the Ser/Thr kinase(s) responsible not determined
    • Stoichiometry and temporal order of Ser/Thr vs. Tyr phosphorylation unclear
  9. 2001 High

    Identification of Y204 as a non-ITAM phosphotyrosine docking site for the SH2 domain of BLNK/SLP-65 revealed how Igα couples proximal Syk activation to distal Ca²⁺ and NF-κB pathways, expanding Igα function beyond classical ITAM signaling.

    Evidence Co-immunoprecipitation after BCR stimulation with SH2–phosphotyrosine mapping; confirmed by chimeric receptor mutagenesis and BLNK fusion reconstitution

    PMID:11449366 PMID:11909947

    Open questions at the time
    • Whether Y176 also recruits BLNK independently of Y204 not fully resolved
    • No crystal structure of Igα tail–BLNK SH2 complex
  10. 2004 High

    Tonic (non-aggregated) Igα/Igβ signals targeted to the inner plasma membrane suffice to drive pre-BCR-dependent developmental checkpoints including κ light chain recombination, establishing that pre-BCR aggregation is dispensable and basal signaling coordinates allelic exclusion.

    Evidence Membrane-targeted cytoplasmic Igα/Igβ construct in primary pro-B cells with IL-7 proliferation, VDJ, and κ recombination readouts

    PMID:15240688

    Open questions at the time
    • Precise signaling threshold distinguishing tonic from activated BCR signaling unknown
    • Which downstream pathways are differentially engaged by tonic vs. aggregated signals not resolved
  11. 2011 High

    CD79A ITAM mutations in ABC-DLBCL were linked to constitutive NF-κB activation and sensitivity to PKC inhibition, establishing a pathogenic gain-of-function mechanism and revealing that oncogenic BCR signaling requires PKC-dependent NF-κB transduction.

    Evidence Cell line sensitivity profiling, NF-κB pathway analysis, cell cycle arrest assays, and xenograft models stratified by CD79A/B mutation status

    PMID:21324920

    Open questions at the time
    • Whether CD79A and CD79B mutations are functionally equivalent or additive not fully dissected
    • Mechanism by which ITAM mutations escape negative regulation not structurally resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the high-resolution structure of the Igα/Igβ heterodimer and its interface with membrane immunoglobulin, the identity of the Ser/Thr kinases that negatively regulate the Igα tail, and the structural basis for asymmetric ITAM tyrosine phosphorylation.
  • No atomic-resolution structure of the complete BCR signaling complex
  • Ser/Thr kinase(s) targeting the Igα cytoplasmic tail remain unidentified
  • Mechanism of Igα cytoplasmic domain oligomerization and its functional significance in vivo not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0060090 molecular adaptor activity 3
Localization
GO:0005886 plasma membrane 4 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-168256 Immune System 7 R-HSA-1266738 Developmental Biology 6 R-HSA-162582 Signal Transduction 5
Partners
BCAP31BLNKCD5CD79BPTPN6SYK
Complex memberships
B-cell antigen receptor (BCR) complex

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 The mb-1 gene (encoding Igα/CD79A) was identified as a B lymphocyte lineage-restricted gene encoding a putative membrane glycoprotein with a leader sequence, extracellular domain, transmembrane portion, and intracellular domain. Antibodies against the mb-1 fusion protein stained pre-B and mature B cell lines on their surface but not T cell lines or fibroblasts, establishing its B-cell-specific surface expression. cDNA cloning, Northern blot, antibody staining of cell lines The EMBO journal High 2463161
1990 The murine mb-1 gene structure was characterized: five exons encoding signal peptide, extracellular, transmembrane, and cytoplasmic domains. A B cell-specific DNase I-hypersensitive site was identified in the 3'-flanking region, indicating its involvement in B cell-specific expression of mb-1. Genomic DNA cloning, Southern blot, DNase I hypersensitivity assay Journal of immunology High 2358676
1991 A common Igα (CD79A) chain associates with all five immunoglobulin classes (IgM, IgD, IgG, IgA, IgE) at the B cell surface. Just two proteins—the alpha and beta associated chains—are sufficient to reconstitute an IgM surface receptor in fibroblasts, demonstrating that the Igα/Igβ heterodimer is the minimal signaling unit of the BCR. Reconstitution in fibroblasts, co-immunoprecipitation, surface receptor expression Nature High 1881434
1992 The 72-kDa protein-tyrosine kinase PTK72 (Syk) is physically associated with the B cell antigen receptor via MB-1 (Igα/CD79A). PTK72 co-immunoprecipitates with sIgM, phosphorylates MB-1 in immune complexes, and its enzymatic activity is activated upon cross-linking of sIgM, placing Syk as an Igα-associated kinase that is activated downstream of BCR engagement. Co-immunoprecipitation, in vitro kinase assay, peptide mapping, reimmunoprecipitation The Journal of biological chemistry High 1569106
1992 Cross-linking of the B cell antigen receptor results in rapid tyrosine phosphorylation of substrate proteins, and the BCR is a multicomponent complex in which membrane-bound Ig is noncovalently associated with an Igα/Igβ heterodimer, establishing the structural basis of BCR-mediated signaling analogous to the T cell receptor/CD3 complex. Biochemical co-immunoprecipitation, tyrosine phosphorylation assays Annual review of immunology High 1591006
1994 CD5 is physically associated with the B cell antigen receptor complex including Igα (CD79A) on human B cells, and CD5 serves as a substrate for BCR-induced tyrosine kinase activity, indicating that CD5+ B cells have a unique capacity to modulate BCR signals. Co-immunoprecipitation, tyrosine phosphorylation assay European journal of immunology Medium 7512031
1995 PTP1C (SHP-1) constitutively associates with the resting BCR complex through co-precipitation with BCR components including Igα. PTP1C specifically dephosphorylates a 35-kDa BCR-associated protein likely representing Igα, and dissociates from the activated BCR complex after receptor engagement, revealing SHP-1 as a phosphatase that regulates the tyrosine phosphorylation state of Igα in resting B cells. Co-immunoprecipitation, phosphatase activity assay, anti-PTP1C antibody depletion The Journal of experimental medicine High 7539038
1995 Both Syk SH2 domains are required for recruitment of Syk to tyrosine-phosphorylated Igα and Igβ ITAMs, and this recruitment is necessary for BCR-mediated Syk and PLCγ2 phosphorylation, IP3 release, and Ca2+ mobilization. The Syk autophosphorylation site Y518/Y519 is required for signal transduction but not for ITAM binding, indicating that ITAM binding precedes and is required for Syk autophosphorylation. Syk knockout B cells reconstituted with Syk mutants, co-immunoprecipitation, calcium flux assay, PLC-γ2 phosphorylation The Journal of experimental medicine High 7500027
1995 Novel variants of mb-1 (CD79A) transcripts generated by alternative mRNA splicing were identified. The variant proteins conserve transmembrane and cytoplasmic portions but lack part of the extracellular domain containing cysteine residues required for disulfide bonds. Transfection studies revealed that variant mb-1 does not contribute to BCR surface expression. B cell activation with anti-IgM, LPS, or IL-4 significantly increases the amount of variant mb-1 transcripts. cDNA cloning, transfection, BCR surface expression assay, Northern blot Immunology letters Medium 8747711
1997 The Igα/Igβ heterodimer is present on the surface of μ-negative proB cell lines in association with calnexin. Cross-linking of Igβ on RAG-2-deficient proB cells induces rapid tyrosine phosphorylation of Igα as well as Syk, PI3-kinase, Vav, SLP-76, and ERK (but not JNK or p38), and induces proB cell differentiation to the small preB cell stage, demonstrating that the Igα/Igβ heterodimer is signaling-competent before μ heavy chain expression. Flow cytometry, anti-Igβ cross-linking in RAG-2-deficient mice, tyrosine phosphorylation analysis, in vivo mAb treatment Immunity High 9354476
1998 Phosphorylation of the two ITAM tyrosines of CD79a (Igα) is asymmetrical: >80% of phosphorylation occurs on the N-terminal tyrosine (Y-E-G-L). Only the N-terminal ITAM tyrosine of CD79a is required for ligand-mediated phosphorylation of the receptor and downstream substrates (p62, p110, Shc), and for Ca2+ mobilization. Both tyrosines are required for Syk phosphorylation. CD79b shows greater dependence on both tyrosines compared to CD79a. MHC class II chimeric receptor system, ITAM tyrosine-to-phenylalanine mutagenesis, phosphorylation assays, Ca2+ mobilization Journal of immunology High 9531288
1999 A homozygous splice defect in Igα (CD79A) in a human patient causes a complete block in B-cell development at the pro-B to pre-B transition, equivalent to that seen in μ heavy chain deficiency, establishing CD79A mutations as a cause of agammaglobulinemia. The block occurs after V-DJ rearrangement, suggesting Igα is not critical for development until expressed as part of the pre-BCR with μ heavy chain. Human patient genetic analysis, immunofluorescence of bone marrow B-cell developmental stages, V-DJ sequencing The Journal of clinical investigation High 10525050
1999 Truncation of the Igα intracellular cytoplasmic domain (mb-1 Δc/Δc mice) results in constitutive signaling of the antigen receptor complex on immature B cells, causing activation and loss of transitional IgMhigh IgDlow B cells, thereby accounting for the paucity of mature peripheral B cells. This demonstrates a negative regulatory role for the Igα cytoplasmic tail during B cell development. mb-1 cytoplasmic tail truncation knock-in mouse, flow cytometry of B-cell developmental stages, analysis of immature B cell activation Immunity High 10591178
2000 All serine and threonine residues in the Igα cytoplasmic tail were mutated to alanine/valine, resulting in stronger tyrosine phosphorylation of Igα and increased BCR signaling upon stimulation. This establishes that serine/threonine kinases negatively regulate ITAM-mediated signal transduction from the BCR by phosphorylating the Igα tail. Site-directed mutagenesis of all Ser/Thr residues, single-chain Fv/Igα chimera and full BCR context, tyrosine phosphorylation assays Proceedings of the National Academy of Sciences of the United States of America High 10900006
2001 SLP-65 (BLNK) directly associates with the BCR signaling subunit via the SH2 domain of SLP-65 binding to phosphorylated Igα tyrosine Y204, which is located outside the ITAM. This identifies a non-ITAM phosphorylation site on Igα as a transmembrane adaptor function coupling the BCR to distal signaling pathways. Co-immunoprecipitation after B cell stimulation, SH2-phosphotyrosine interaction mapping European journal of immunology High 11449366
2002 BLNK is directly recruited to Igα via non-ITAM tyrosines Y176 and Y204. Using chimeric receptors with wild-type and mutant Igα cytoplasmic tails, Y204 was shown to bind BLNK directly, and fusion of BLNK to mutated Igα reconstituted downstream signaling. BCR ligation induces Y204 phosphorylation and BLNK recruitment, establishing the molecular mechanism by which Igα couples Syk activation to BLNK-dependent pathways. Chimeric receptor mutagenesis, direct binding assays, reconstitution of signaling in mutant-Igα expressing cells Molecular and cellular biology High 11909947
2003 The mb-1 (Igα/CD79A) gene undergoes somatic hypermutation (SHM) in germinal center B cells at frequencies similar to other non-Ig genes but lower than Ig genes. Mutations in mb-1 occur as single nucleotide substitutions targeted to hotspots, with a characteristic distribution pattern across the gene, identifying CD79A as a target of the SHM machinery during B cell maturation. Sequencing of mb-1 genes from GC-derived malignant B cell lines and normal peripheral B cells, SHM hotspot analysis Proceedings of the National Academy of Sciences of the United States of America High 12651942
2003 BAP29 and BAP31 ER-resident membrane proteins bind to membrane-bound IgD in the ER and retain it there; this retention is distinct from and competitive with Igα/Igβ binding to mIgD. Only a minor fraction of intracellular mIgD is associated with BAP29/BAP31 complexes. Coexpression of BAP29/BAP31 prevented aberrant surface transport of mIgD in the absence of Igα/Igβ, establishing that BAP complexes function as ER retention proteins for mIg that is not assembled with Igα/Igβ. Blue native PAGE, co-immunoprecipitation, Drosophila S2 cell surface expression, chimeric mIgD constructs Proceedings of the National Academy of Sciences of the United States of America High 12886015
2004 The cytoplasmic domain of Igα (CD79A) forms stable dimers and tetramers in solution even below 10 μM, in contrast to other ITAM-containing proteins. Circular dichroic analysis reveals that the Igα cytoplasmic domain lacks stable ordered structure (random-coil-like), and phosphorylation does not significantly alter oligomerization behavior, suggesting a structural basis for transmembrane signal initiation. Purified recombinant Igα cytoplasmic domain, biophysical assays (sedimentation, CD spectroscopy), NMR, phosphorylation analysis Biochemistry High 14967045
2004 Basal signaling through non-aggregated Igα/Igβ complexes targeted to the inner plasma membrane leaflet of primary pro-B cells is sufficient to promote pre-BCR-dependent processes: enhanced proliferation at low IL-7, suppression of VH(D)JH recombination, and induction of κ light chain recombination and cytoplasmic κ expression. This demonstrates that pre-BCR aggregation is not required for pre-BCR function and that tonic Igα/Igβ signals coordinate developmental checkpoints. Membrane-targeted cytoplasmic Igα/Igβ construct in primary pro-B cells, IL-7 proliferation assay, VDJ/κ recombination analysis Journal of immunology High 15240688
2004 The cytoplasmic domain of avian Igα (CD79A ortholog) efficiently supports B-cell development in precursors lacking endogenous sIg when expressed as a chimeric CD8α-Igα(cyt) receptor, whereas an equivalent chimeric receptor containing the Igβ cytoplasmic domain actively inhibited B-cell development. This establishes functionally distinct roles for the Igα and Igβ cytoplasmic domains in B-cell development. Retroviral gene transfer of chimeric receptor constructs into chicken B-cell precursors in vivo, B-cell development assay Immunological reviews High 14962183
2006 The mb-1 gene (encoding Igα/CD79A) was used as a host locus for Cre recombinase to generate mb1-cre mice. Integration of humanized Cre into the mb1 locus results in extraordinarily efficient recombination of loxP sites exclusively in the B cell lineage beginning at the very early pro-B cell stage, confirming that mb-1/CD79A expression initiates at the earliest B-cell progenitor stage. Knock-in of humanized Cre into mb1 locus, reporter gene analysis across B-cell developmental stages Proceedings of the National Academy of Sciences of the United States of America High 16940357
2007 The Igα ITAM is required for efficient pre-B cell differentiation but not for pre-BCR-induced proliferation. Reconstitution of Igα tyrosine mutants in SLP-65/Igα double-deficient pre-B cells showed comparable pre-BCR surface expression but different signaling (tyrosine phosphorylation, calcium flux); the ITAM tyrosines and Y204 are required for efficient calcium flux and differentiation. Additionally, the pre-BCR modulates IL-7 receptor surface expression, increasing IL-7 sensitivity. Igα mutant reconstitution in double-deficient pre-B cells, proliferation and differentiation assays, calcium flux, flow cytometry European journal of immunology High 17163454
2007 Anti-CD79b antibody-drug conjugates (ADCs) are trafficked to the lysosomal-like MHC class II-positive compartment (MIIC) following BCR internalization. Anti-CD79b ADCs with stable linkers were effective in killing NHL cell lines in vitro and in xenograft models. Anti-CD79b ADCs downregulated surface BCR, while anti-CD79a ADCs were less effective, suggesting differential intracellular trafficking between CD79a and CD79b upon BCR engagement. ADC cytotoxicity assays in NHL cell lines, xenograft mouse models, confocal microscopy of lysosomal trafficking, BCR downregulation assay Blood Medium 17374736
2011 CD79A/CD79B mutations in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) correlate with sensitivity to the PKC inhibitor sotrastaurin (STN). PKC inhibition in CD79A/B-mutant cells blocks NF-κB pathway activity, induces G1-phase cell-cycle arrest and/or cell death, and produces significant antitumor effects in a xenograft model, establishing that CD79A mutations drive constitutive NF-κB activation via PKC-dependent BCR signaling. Cell line sensitivity profiling, NF-κB pathway analysis, cell cycle assay, xenograft mouse model Cancer research High 21324920
2021 A composite CD79A/CD40 co-stimulatory endodomain incorporated into CD19-CAR T cells (CD19.79a.40z) induces higher NF-κB and p38 activity upon CD19 antigen exposure compared to CD28 or 4-1BB co-stimulatory domains. CD19.79a.40z CAR-T cells exhibit robust T cell proliferation independent of exogenous IL-2, sustained tumor suppression in co-culture, and superior anti-tumor activity with enhanced in vivo CAR-T cell proliferation in Raji-inoculated mice, demonstrating that the CD79A intracellular domain can activate NF-κB signaling and enhance T cell function as a co-stimulatory module. CAR-T cell co-culture cytotoxicity assays, NF-κB/p38 reporter assays, in vitro proliferation, Raji xenograft mouse model Molecular therapy High 33940156
2023 CD79a/CD79b mediate BCR signal initiation and transduction through ITAMs, with post-translational modifications (phosphorylation of ITAM tyrosines, serine/threonine phosphorylation) regulating signaling. CD79A/CD79B mutations in lymphoid neoplasms, particularly ABC-DLBCL, cause constitutive BCR signaling through chronic active BCR signaling. CD79a functions as a signal integrator within the BCR complex, with its non-ITAM tyrosines (Y176, Y204) serving as adaptor sites for BLNK/SLP-65 recruitment, and its cytoplasmic tail regulating signal amplitude through serine/threonine phosphorylation. Review synthesizing ITAM mutagenesis, structural, interactome, and lymphoma mutation studies International journal of molecular sciences Medium 38203179

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2011 Secretory IgA's complex roles in immunity and mucosal homeostasis in the gut. Mucosal immunology 914 21975936
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 The pathophysiology of IgA nephropathy. Journal of the American Society of Nephrology : JASN 681 21949093
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2006 Testing gene function early in the B cell lineage in mb1-cre mice. Proceedings of the National Academy of Sciences of the United States of America 497 16940357
1994 Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. Gene 492 8125298
1992 Antigen receptors on B lymphocytes. Annual review of immunology 437 1591006
2001 IgA Fc receptors. Annual review of immunology 389 12524384
2010 Selective IgA deficiency. Journal of clinical immunology 362 20101521
1966 The IgA system. I. Studies of the transport and immunochemistry of IgA in the saliva. The Journal of experimental medicine 319 4160397
1988 B lymphocyte lineage-restricted expression of mb-1, a gene with CD3-like structural properties. The EMBO journal 295 2463161
2001 Predicting progression in IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 291 11576875
1992 Association of the 72-kDa protein-tyrosine kinase PTK72 with the B cell antigen receptor. The Journal of biological chemistry 287 1569106
1991 The B-cell antigen receptor of the five immunoglobulin classes. Nature 267 1881434
2018 IgA Responses to Microbiota. Immunity 264 30134201
2004 An investigation into the human serum "interactome". Electrophoresis 247 15174051
1995 Identification of the tyrosine phosphatase PTP1C as a B cell antigen receptor-associated protein involved in the regulation of B cell signaling. The Journal of experimental medicine 224 7539038
2001 IgA and the IgA Fc receptor. Trends in immunology 221 11274926
1995 Role of the Syk autophosphorylation site and SH2 domains in B cell antigen receptor signaling. The Journal of experimental medicine 218 7500027
1985 Jacalin: an IgA-binding lectin. Journal of immunology (Baltimore, Md. : 1950) 215 3871459
2019 IgA: Structure, Function, and Developability. Antibodies (Basel, Switzerland) 195 31817406
2012 Pathogenesis of IgA nephropathy. Nature reviews. Nephrology 184 22430056
2014 The genetics and immunobiology of IgA nephropathy. The Journal of clinical investigation 174 24892706
2009 Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip. American journal of human genetics 164 19913121
2023 IgA nephropathy. Nature reviews. Disease primers 153 38036542
1995 CD79a: a novel marker for B-cell neoplasms in routinely processed tissue samples. Blood 151 7632952
1999 Mutations in Igalpha (CD79a) result in a complete block in B-cell development. The Journal of clinical investigation 147 10525050
2012 Corticosteroid therapy in IgA nephropathy. Journal of the American Society of Nephrology : JASN 142 22539830
1988 The immunohistology of IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 134 3142256
2007 Antibody-drug conjugates targeted to CD79 for the treatment of non-Hodgkin lymphoma. Blood 129 17374736
2021 IgA vasculitis. Seminars in immunopathology 115 34170395
2021 Current treatment of IgA nephropathy. Seminars in immunopathology 112 34495361
2006 Treatment of IgA nephropathy. Kidney international 112 16641928
2004 Homooligomerization of the cytoplasmic domain of the T cell receptor zeta chain and of other proteins containing the immunoreceptor tyrosine-based activation motif. Biochemistry 110 14967045
2002 Interactions of human mesangial cells with IgA and IgA-containing immune complexes. Kidney international 109 12110007
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
2001 Association of SLP-65/BLNK with the B cell antigen receptor through a non-ITAM tyrosine of Ig-alpha. European journal of immunology 106 11449366
2014 IgA, IgA receptors, and their anti-inflammatory properties. Current topics in microbiology and immunology 104 25116102
1994 CD5 is associated with the human B cell antigen receptor complex. European journal of immunology 103 7512031
2004 Pathogenesis of IgA nephropathy. Seminars in nephrology 100 15156526
2011 Protein kinase C inhibitor sotrastaurin selectively inhibits the growth of CD79 mutant diffuse large B-cell lymphomas. Cancer research 96 21324920
2007 TACI regulates IgA production by APRIL in collaboration with HSPG. Blood 93 17119122
2002 The direct recruitment of BLNK to immunoglobulin alpha couples the B-cell antigen receptor to distal signaling pathways. Molecular and cellular biology 92 11909947
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
1988 Proteinuria in IgA nephropathy. Kidney international 88 3367561
2014 Re-thinking the functions of IgA(+) plasma cells. Gut microbes 87 25483334
2021 Complement activation in IgA nephropathy. Seminars in immunopathology 86 34379175
2013 The HIV-1 envelope protein gp120 impairs B cell proliferation by inducing TGF-β1 production and FcRL4 expression. Nature immunology 84 24162774
2004 PAX5 expression in acute leukemias: higher B-lineage specificity than CD79a and selective association with t(8;21)-acute myelogenous leukemia. Cancer research 83 15492262
1991 IgA deficiency. Immunodeficiency reviews 80 1931006
1998 Co-expression of CD79a (JCB117) and CD3 by lymphoblastic lymphoma. The Journal of pathology 79 9924428
1988 Circulating complexes containing IgA and fibronectin in patients with primary IgA nephropathy. Proceedings of the National Academy of Sciences of the United States of America 78 3387443
1999 Identification of residues in the CH2/CH3 domain interface of IgA essential for interaction with the human fcalpha receptor (FcalphaR) CD89. The Journal of biological chemistry 77 10438530
1983 Isolation of human complex-forming glycoprotein, heterogeneous in charge (protein HC), and its IgA complex from plasma. Physiochemical and immunochemical properties, normal plasma concentration. The Journal of biological chemistry 76 6196366
1997 Prothrombin, albumin and immunoglobulin A form covalent complexes with alpha1-microglobulin in human plasma. European journal of biochemistry 75 9183005
2003 A high-molecular-weight complex of membrane proteins BAP29/BAP31 is involved in the retention of membrane-bound IgD in the endoplasmic reticulum. Proceedings of the National Academy of Sciences of the United States of America 74 12886015
1996 Localization of the binding site for the monocyte immunoglobulin (Ig) A-Fc receptor (CD89) to the domain boundary between Calpha2 and Calpha3 in human IgA1. The Journal of experimental medicine 72 8666916
1998 Asymmetrical phosphorylation and function of immunoreceptor tyrosine-based activation motif tyrosines in B cell antigen receptor signal transduction. Journal of immunology (Baltimore, Md. : 1950) 71 9531288
1994 Expression of J chain mRNA in duodenal IgA plasma cells in IgA nephropathy. Kidney international 71 8196286
1986 Evidence for IgA-specific B cell hyperactivity in patients with IgA nephropathy. Kidney international 70 3486314
2010 New genetic associations detected in a host response study to hepatitis B vaccine. Genes and immunity 69 20237496
1990 Structure of the murine mb-1 gene encoding a putative sIgM-associated molecule. Journal of immunology (Baltimore, Md. : 1950) 69 2358676
1987 Complement activation in IgA nephropathy. Kidney international 68 3586493
1988 Activation of complement by human serum IgA, secretory IgA and IgA1 fragments. Molecular immunology 66 3173354
2009 Role of IgA and IgA fc receptors in inflammation. Journal of clinical immunology 65 19834792
1992 Receptors for IgA on phagocytic cells. Immunologic research 64 1287121
2000 Immunoreactivity of B-cell markers (CD79a, L26) in rare cases of extranodal cytotoxic peripheral T- (NK/T-) cell lymphomas. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 63 10912936
1983 Inhibition of microbial IgA proteases by human secretory IgA and serum. Molecular immunology 62 6417473
2014 MicroRNAs in IgA nephropathy. Nature reviews. Nephrology 61 24709842
2011 IgA pemphigus. Clinics in dermatology 60 21679872
2002 Pathogenic significance of IgA receptor interactions in IgA nephropathy. Trends in molecular medicine 59 12383768
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
2015 Role of complement in IgA nephropathy. Journal of nephrology 58 26567162
2006 IgA-containing immune complexes in the urine of IgA nephropathy patients. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 55 16757497
1988 Activation of complement in IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 52 3055972
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