Product nameAnti-CD79a antibody [EPR3619]
See all CD79a primary antibodies
DescriptionRabbit monoclonal [EPR3619] to CD79a
Tested applicationsSuitable for: WB, ICC/IF, Flow Cytmore details
Unsuitable for: IHC-P or IP
Species reactivityReacts with: Human
Synthetic peptide corresponding to residues in Human CD79a (UniProt ID: P11912)
- Raji cell lysate. Ramos cells.
Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.05% Sodium azide
Constituents: 0.1% BSA, 40% Glycerol, 9.85% Tris glycine, 50% Tissue culture supernatant
PurityTissue culture supernatant
Our Abpromise guarantee covers the use of ab133483 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 25 kDa.|
|ICC/IF||1/250 - 1/500.|
|Flow Cyt||1/100 - 1/500.
ab172730 - Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.
FunctionRequired in cooperation with CD79B for initiation of the signal transduction cascade activated by binding of antigen to the B-cell antigen receptor complex (BCR) which leads to internalization of the complex, trafficking to late endosomes and antigen presentation. Also required for BCR surface expression and for efficient differentiation of pro- and pre-B-cells. Stimulates SYK autophosphorylation and activation. Binds to BLNK, bringing BLNK into proximity with SYK and allowing SYK to phosphorylate BLNK. Also interacts with and increases activity of some Src-family tyrosine kinases. Represses BCR signaling during development of immature B cells.
Involvement in diseaseDefects in CD79A are the cause of agammaglobulinemia type 3 (AGM3) [MIM:613501]. It is a primary immunodeficiency characterized by profoundly low or absent serum antibodies and low or absent circulating B cells due to an early block of B-cell development. Affected individuals develop severe infections in the first years of life. Note=Two different mutations, one at the splice donor site of intron 2 and the other at the splice acceptor site for exon 3, have been identified. Both mutations give rise to a truncated protein.
Sequence similaritiesContains 1 Ig-like C2-type (immunoglobulin-like) domain.
Contains 1 ITAM domain.
modificationsPhosphorylated on tyrosine, serine and threonine residues upon B-cell activation. Phosphorylation of tyrosine residues by Src-family kinases is an early and essential feature of the BCR signaling cascade. The phosphorylated tyrosines serve as docking sites for SH2-domain containing kinases, leading to their activation which in turn leads to phosphorylation of downstream targets. Phosphorylation of serine and threonine residues may prevent subsequent tyrosine phosphorylation.
Cellular localizationCell membrane. Following antigen binding, the BCR has been shown to translocate from detergent-soluble regions of the cell membrane to lipid rafts although signal transduction through the complex can also occur outside lipid rafts.
- Information by UniProt
- B lymphocyte-specific MB1 protein antibody
- B-cell antigen receptor complex-associated protein alpha chain antibody
- CD 79a antibody
All lanes : Anti-CD79a antibody [EPR3619] (ab133483) at 1/1000 dilution
Lane 1 : Raji cell lysate
Lane 2 : Ramos cell lysate
Lysates/proteins at 10 µg per lane.
All lanes : HRP labelled goat anti-rabbit at 1/2000 dilution
Predicted band size: 25 kDa
Flow cytometric analysis of permeabilised Ramos cells labelled with ab133483 at 1/100 dilution (red) or negative rabbit IgG (green).
ab133483 has not yet been referenced specifically in any publications.