|Recombinant Human BLNK / Ly-57 / SLP-65 protein (Catalog#12706-H07H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Human BLNK / Ly-57 / SLP-65 (rh BLNK / Ly-57 / SLP-65; Catalog#12706-H07H; P08195-1; Met 1-Ser 456). BLNK / Ly-57 / SLP-65 specific IgG was purified by Human BLNK / Ly-57 / SLP-65 affinity chromatography.|
|Human BLNK / Ly-57 / SLP-65|
|WB, ELISA, IHC-P|
WB: 10-20 μg/mL
ELISA: 0.1-0.2 μg/mL
This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human BLNK. The detection limit for Human BLNK is approximately 0.039 ng/well.
IHC-P: 0.1-2 μg/mL
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
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.