7wsp

</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7wsp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7wsp OCA], [https://pdbe.org/7wsp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7wsp RCSB], [https://www.ebi.ac.uk/pdbsum/7wsp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7wsp ProSAT]</span></td></tr>

== Disease ==

[https://www.uniprot.org/uniprot/CD79A_HUMAN CD79A_HUMAN] Autosomal agammaglobulinemia. The disease is caused by variants affecting the gene represented in this entry. 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.

== Function ==

[https://www.uniprot.org/uniprot/CD79A_HUMAN CD79A_HUMAN] Required 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.<ref>PMID:8617796</ref> <ref>PMID:9057631</ref>

== References ==

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