All BLNK reagents are produced in house and quality controlled, including 3 BLNK Antibody, 15 BLNK Gene, 1 BLNK Lysate, 1 BLNK Protein. All BLNK reagents are ready to use.
Recombinant BLNK proteins are expressed by HEK293 Cells with fusion tags as N-His.
BLNK antibodies are validated with different applications, which are ELISA, WB, IHC-P.
BLNK cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each BLNK of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
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.
Fu C., et al., 1998, Immunity 9:93-103.
Minegishi Y., et al., 1999, Science 286:1954-1957.