an adaptor protein that bridges the B-cell receptor-associated kinases (BCR) with a multitude of signaling pathways, regulating biologic outcomes of B-cell function and development. Plays an important role in BCR-mediated PLCG1 activation and Ca(2 ) mobilization. Does not seem to be not required for pre-BCR-mediated activation of MAP kinase and phosphatidyl-inositol 3 (PI3) kinase signaling. Plays a critical role in orchestrating the pro-B cell to pre-B cell transition. 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. Its phosphorylation is required for both Ca(2 ) and MAPK signaling pathways. Defects in BLNK are the cause of hypoglobulinemia and absent B-cells.It has tumor supressor activity that is lost in many cases of childhood pre-B acute lymphoblastic leukemia (ALL). Two alternatively spliced isoforms have been described; these are differentially involved in activation and apoptosis of B lymphocytes. Note: This description may include information from UniProtKB.
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.