|Application ||WB, E|
|Other Accession||NP_001706.2, 640|
|Calculated MW||57706 Da|
|Other Names||Tyrosine-protein kinase Blk, 188.8.131.52, B lymphocyte kinase, p55-Blk, BLK|
|Format||0.5 mg/ml in Tris saline, 0.02% sodium azide, pH7.3 with 0.5% bovine serum albumin|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||BLK Antibody (N-Term, near) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Non-receptor tyrosine kinase involved in B-lymphocyte development, differentiation and signaling. B-cell receptor (BCR) signaling requires a tight regulation of several protein tyrosine kinases and phosphatases, and associated coreceptors. Binding of antigen to the B-cell antigen receptor (BCR) triggers signaling that ultimately leads to B-cell activation. Signaling through BLK plays an important role in transmitting signals through surface immunoglobulins and supports the pro-B to pre-B transition, as well as the signaling for growth arrest and apoptosis downstream of B-cell receptor. Specifically binds and phosphorylates CD79A at 'Tyr-188'and 'Tyr-199', as well as CD79B at 'Tyr-196' and 'Tyr- 207'. Phosphorylates also the immunoglobulin G receptors FCGR2A, FCGR2B and FCGR2C. With FYN and LYN, plays an essential role in pre-B-cell receptor (pre-BCR)-mediated NF-kappa-B activation. Contributes also to BTK activation by indirectly stimulating BTK intramolecular autophosphorylation. In pancreatic islets, acts as a modulator of beta-cells function through the up-regulation of PDX1 and NKX6-1 and consequent stimulation of insulin secretion in response to glucose.|
|Cellular Location||Cell membrane; Lipid-anchor. Note=Present and active in lipid rafts. Membrane location is required for the phosphorylation of CD79A and CD79B (By similarity).|
|Tissue Location||Expressed in lymphatic organs, pancreatic islets, Leydig cells, striate ducts of salivary glands and hair follicles.|
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Isoforms of the Ets transcription factor NERF/ELF-2 physically interact with AML1 and mediate opposing effects on AML1-mediated transcription of the B cell-specific blk gene. Cho JY, Akbarali Y, Zerbini LF, Gu X, Boltax J, Wang Y, Oettgen P, Zhang DE, Libermann TA, The Journal of biological chemistry 2004 May 279 (19): 19512-22. PMID: 14970218
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