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BLNK/Ly-57/SLP-65  Protein, Antibody, ELISA Kit, cDNA Clone

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Expression host: Human Cells  
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BLNK/Ly-57/SLP-65 Related Area

BLNK/Ly-57/SLP-65 Related Pathways

BLNK/Ly-57/SLP-65 Related Protein, Antibody, cDNA Gene, and ELISA Kits

BLNK/Ly-57/SLP-65 Summary & Protein Information

BLNK/Ly-57/SLP-65 Background

Gene Summary: This gene encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. This protein bridges B cell receptor-associated kinase activation with downstream signaling pathways, thereby affecting various biological functions. The phosphorylation of five tyrosine residues is necessary for this protein to nucleate distinct signaling effectors following B cell receptor activation. Mutations in this gene cause hypoglobulinemia and absent B cells, a disease in which the pro- to pre-B-cell transition is developmentally blocked. Deficiency in this protein has also been shown in some cases of pre-B acute lymphoblastic leukemia. Alternatively spliced transcript variants have been found for this gene
General information above from NCBI
Subunit structure: Associates with PLCG1, VAV1 and NCK1 in a B-cell antigen receptor-dependent fashion. Interacts with VAV3, PLCG2 and GRB2. Interacts through its SH2 domain with CD79A. Interacts (via SH2 domain) with SYK; phosphorylated and activated by SYK. Interacts with SCIMP. {ECO:0000269|PubMed:16912232, ECO:0000269|PubMed:18369315, ECO:0000269|PubMed:21930792, ECO:0000269|PubMed:9341187, ECO:0000269|PubMed:9697839}.
Subcellular location: Cytoplasm {ECO:0000269|PubMed:9697839}. Cell membrane {ECO:0000269|PubMed:9697839}. Note=BCR activation results in the translocation to membrane fraction.
Tissue specificity: Expressed in B-cell lineage and fibroblast cell lines (at protein level). Highest levels of expression in the spleen, with lower levels in the liver, kidney, pancreas, small intestines and colon.
Post-translational: Following BCR activation, phosphorylated on tyrosine residues by SYK and LYN. When phosphorylated, serves as a scaffold to assemble downstream targets of antigen activation, including PLCG1, VAV1, GRB2 and NCK1. Phosphorylation of Tyr-84, Tyr-178 and Tyr-189 facilitates PLCG1 binding. Phosphorylation of Tyr-96 facilitates BTK binding. Phosphorylation of Tyr-72 facilitates VAV1 and NCK1 binding. Phosphorylation is required for both Ca(2+) and MAPK signaling pathways. {ECO:0000269|PubMed:12456653, ECO:0000269|PubMed:9697839}.
Involvement in disease: DISEASE: Agammaglobulinemia 4, autosomal recessive (AGM4) [MIM:613502]: 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. {ECO:0000269|PubMed:10583958}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Contains 1 SH2 domain. {ECO:0000255|PROSITE-ProRule:PRU00191}.
General information above from UniProt

B-cell linker protein, also known as B-cell adapter containing a SH2 domain protein, B-cell adapter containing a Src homology 2 domain protein, Cytoplasmic adapter protein, Src homology 2 domain-containing leukocyte protein of 65 kDa, SLP-65 and BLNK, is a cytoplasm and cell membrane protein which contains one SH2 domain. BLNK is expressed in B-cell lineage and fibroblast cell lines. Highest levels of expression is in the spleen, with lower levels in the liver, kidney, pancreas, small intestines and colon. BLNK functions as a central linker protein that bridges kinases associated with the B-cell receptor (BCR) with a multitude of signaling pathways, regulating biological outcomes of B-cell function and development. BLNK plays a role in the activation of ERK / EPHB2, MAP kinase p38 and JNK. BLNK modulates AP1 activation. It is important for the activation of NF-kappa-B and NFAT. BLNK plays an important role in BCR-mediated PLCG1 and PLCG2 activation and Ca2+ mobilization and is required for trafficking of the BCR to late endosomes. BLNK may be required for the RAC1-JNK pathway. It plays a critical role in orchestrating the pro-B cell to pre-B cell transition. BLNK also plays an important role in BCR-induced B-cell apoptosis. Defects in BLNK are the cause of agammaglobulinemia type 4 (AGM4) which 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.

BLNK/Ly-57/SLP-65 Alternative Name

bca,AGM4,BASH,LY57,SLP65,BLNK-S,SLP-65, [homo-sapiens]
BASH,BLNK,BLNK-S,LY57,Ly-57,MGC111051,SLP65,SLP-65, [human]
BASH,Bca,Blnk,Ly57,Ly-57,Lyw-57,SLP-65, [mouse]
Bca,BASH,Ly57,Ly-57,Lyw-57,SLP-65, [mus-musculus]

BLNK/Ly-57/SLP-65 Related Studies

  • Fu C., et al., 1998, Immunity 9:93-103.
  • Minegishi Y., et al., 1999, Science 286:1954-1957.
  • Chiu C.W., et al., 2002, EMBO J. 21:6461-6472.
  • Taguchi T., et al., 2004, Immunology 112:575-582.