Disease relevance of Cd79a

• The transcription factor Pax5 activated endogenous mb-1 transcription in a plasmacytoma cell line, but could not when the promoter was methylated [1].
• We first verified whether BCR-associated Ig alpha translocates to the cytoskeleton together with mIgM in polyclonal anti-IgM-treated murine B lymphoma cell line, BAL17.7 [2].
• Five acquired immunodeficiency syndrome (AIDS)-MLs and ten SCID-EBV-positive BMLs were first analysed by immunohistochemistry for the expression of Mb-1, B29 and Lyn [3].
• The expression of the B-cell marker mb-1 (CD79a) in Hodgkin's disease [4].

Psychiatry related information on Cd79a

• Resulting Thyl-2+, L3T4+ cell lines depend on the T15 Id+ BCg3R-1d cells for growth and demonstrate the ability to bind TEPC15, a S107 germline-encoded, PC-specific Ig alpha [5].

High impact information on Cd79a

• Early B-cell factor (EBF) is a cell type-specific transcription factor that is expressed at all antigen-independent stages of B-lymphocyte differentiation and participates in the regulation of the mb-1 gene [6].
• Crosslinking Fc gamma RIIB with the surface immunoglobulin complex confers a dominant signal that prevents or aborts lymphocyte activation triggered through the ARH-1 motifs of the signal transduction subunits Ig-alpha and Ig-beta [7].
• This inhibition is directly coupled to signalling mediated through Ig-alpha and Ig-beta as evidenced by chimaeric IgM/alpha and IgM/beta molecules [7].
• A transfection experiment indicates that IgM-alpha is the product of mb-1, a B-cell specific gene encoding a transmembrane protein with sequence homology to proteins of the T-cell antigen receptor-CD3 complex [8].
• Hence, Ig-alpha/beta are used in a sequential fashion for transduction of antigen and cognate T cell help signals [9].

Chemical compound and disease context of Cd79a

• To determine whether a signal-competent Ig complex can already be assembled in the ER, we analyzed the consequence of pervanadate on tyrosine phosphorylation of Ig alpha in J558L plasmacytoma and 38B9 pre-B cells transfected with either a transport-competent IgL chain-pairing or an ER-retained nonpairing micro HC [10].

Biological context of Cd79a

• In contrast, the expression of the mb-1 and LEF-1 genes was already reconstituted by the paired domain polypeptide lacking any transactivation function, suggesting that the DNA-binding domain of BSAP is sufficient to recruit other transcription factors to the regulatory regions of these two genes [11].
• Here, we used in vivo footprinting assays to detect occupation of binding sites in endogenous mb-1 promoters at various stages of B-cell differentiation [12].
• In transfection assays, selective methylation of a single CpG within the Pax-5-dependent Ets site greatly reduces mb-1 promoter activity [13].
• Although B-lineage cells have only unmethylated mb-1 genes and do not modulate methylation of the mb-1 promoter during development, other tissues feature high percentages of methylated alleles [13].
• These results point to the importance of the mIgM transmembrane region in mediating binding to accessory molecules, and provide support for a role of Ig-alpha and Ig-beta/gamma that extends beyond surface expression to signal transduction in B lymphocytes [14].

Anatomical context of Cd79a

• The Ig alpha/Igbeta heterodimer on mu-negative proB cells is competent for transducing signals to induce early B cell differentiation [15].
• The early B cell-specific mb-1 promoter was hypermethylated at CpG dinucleotides in hematopoietic stem cells but became progressively unmethylated as B cell development proceeded [1].
• Ig alpha/Ig beta complexes generate signals for B cell development independent of selective plasma membrane compartmentalization [16].
• A gene, called m-mb-1, was isolated from a murine pre-B-minus T lymphocyte subtracted library [17].
• Antibodies raised against a fusion protein of m-mb-1 with protein A, affinity purified for their m-mb-1 specificity, stained pre-B and mature B cell lines on their surface, but did not stain T cell lines and fibroblasts [17].

Associations of Cd79a with chemical compounds

• Ig beta Delta C mice differ from Ig alpha Delta C mice in that they show little impairment in early B cell development and they produce immature B cells that respond normally to BCR cross-linking as determined by Ca(2+) flux [18].
• Analysis of Ig-alpha-tyrosine kinase interaction reveals two levels of binding specificity and tyrosine phosphorylated Ig-alpha stimulation of Fyn activity [19].
• The nucleotide sequence of the m-mb-1 gene encodes a putative membrane glycoprotein with 220 amino acids, which includes a leader sequence, a putative extracellular domain with two potential N-glycosylation sites, a transmembrane portion and a putative intracellular domain [17].
• In addition, these data indicate that the hydroxyl groups of the mutated residues are not required for functional association between mu and Ig-alpha/Ig-beta because their removal did not reduce the ability of the YS/FA mutant mIgM to associate with accessory proteins or to participate in signal transduction [20].
• As expected, however, PTPs modulate the phosphorylation state of these proteins since another PTP inhibitor, phenylarsine oxide (PAO), increased phosphorylation of Ig-alpha, Ig-beta and other proteins in this system [21].

Physical interactions of Cd79a

• In vivo, Id proteins modulate the transcriptional activity mediated by Pax-5 complexes on the B-cell-specific mb-1 promoter [22].

Enzymatic interactions of Cd79a

• Syk protein-tyrosine kinase is regulated by tyrosine-phosphorylated Ig alpha/Ig beta immunoreceptor tyrosine activation motif binding and autophosphorylation [23].
• Consistent with the proposed role for src family tyrosine kinases in AgR signaling, we found that Lck could phosphorylate the cytoplasmic tails of the Ig-alpha and Ig-beta components of the B cell AgR in vitro [24].

Regulatory relationships of Cd79a

• The mb-1 (Igalpha) gene is B cell-specific and expressed throughout B cell maturation [25].

Other interactions of Cd79a

• Early B cell factor cooperates with Runx1 and mediates epigenetic changes associated with mb-1 transcription [1].
• EBF and the basic helix-loop-helix transcription factor E47 each contributed to epigenetic modifications of the mb-1 promoter, including CpG demethylation and nucleosomal remodeling [1].
• Although lambda5 and Ig-alpha are not expressed, the mu 0 and I mu transcripts from the unrearranged IgH locus are expressed early, in distinct patterns, then repressed just before RAG1 expression [26].
• The promoter region lacks a TATA element, but contains two copies of an early B cell factor-binding motif, which previously has been shown to be important for murine mb-1 expression [27].
• The mb-1 gene encodes the Ig-alpha component of the B-cell antigen receptor [28].

Analytical, diagnostic and therapeutic context of Cd79a

• The monomer MB-1 and Ig-alpha in the pre-B cell line were shown to migrate with identical patterns in nonequilibrium pH gradient gel electrophoresis/SDS-PAGE [29].
• The mb-1 gene was localized to chromosome 19q13.2-13.3 by a combination of two methods, PCR amplification of DNA from a somatic cell hybrid-mapping panel and fluorescence in situ hybridization [27].
• Southern blot analysis of genomic liver DNA with the cloned mb-1 cDNA suggests the existence of another mb-1-related gene segment [30].
• Recombinant mouse EBF binds to the PyG site with an affinity about 3-fold lower than to the EBF binding site from the mouse mb-1 promoter in electrophoretic mobility shift assays [31].
• Many of the cell fate decisions in precursor B cells and more mature B cells are controlled by membrane immunoglobulin (Ig)M heavy chain (mu) and the Ig alpha-Ig beta signal transducers [32].

References