Anti-Human BLNK Antibody Pair

Product Description: B cell linker (BLNK), also known as SLP-65, BASH, and BCA, is a cytoplasmic adaptor protein crucial for B cell development and receptor signaling. It lacks intrinsic enzymatic activity but plays a pivotal role in coordinating and regulating downstream signaling effectors in B cell receptor (BCR) signaling. BLNK consists of a N-terminal leucine zipper motif, an acidic region, a proline-rich region, and a C-terminal SH2 domain, which allows it to localize to the plasma membrane and interact with various signaling proteins. Phosphorylation of BLNK by Syk tyrosine kinase provides docking sites for SH2-containing effector molecules such as Grb2, PLCgamma2, Btk, Vav, and Nck, facilitating the activation of their respective signaling pathways. Deficiency in BLNK leads to impaired B cell development, with knockout mice showing a partial block and humans exhibiting a more profound block in B cell development. Additionally, BLNK may have tumor suppressive activity through its interaction with Bruton's tyrosine kinase (Btk) and regulation of the pre-B cell checkpoint. Protein Function: Functions as a central linker protein, downstream of the B-cell receptor (BCR), bridging the SYK kinase to a multitude of signaling pathways and regulating biological outcomes of B-cell function and development. Plays a role in the activation of ERK/EPHB2, MAP kinase p38 and JNK. Modulates AP1 activation. Important for the activation of NF-kappa-B and NFAT. Plays an important role in BCR-mediated PLCG1 and PLCG2 activation and Ca(2+) mobilization and is required for trafficking of the BCR to late endosomes. However, does not seem to be required for pre-BCR-mediated activation of MAP kinase and phosphatidyl-inositol 3 (PI3) kinase signaling. May be required for the RAC1-JNK pathway. Plays a critical role in orchestrating the pro-B cell to pre-B cell transition. May play an important role in BCR-induced B-cell apoptosis [The Uniprot Consortium]