Target：BLNK
Fields：NF-kappa B signaling pathway;Osteoclast differentiation;B cell receptor signaling pathway;Epstein-Barr virus infection;Primary immunodeficiency
Gene Name：BLNK
Protein Name：B-cell linker protein
Human Gene Id：29760
Human Swiss Prot No：Q8WV28
Mouse Gene Id：17060
Mouse Swiss Prot No：Q9QUN3
Immunogen：The antiserum was produced against synthesized peptide derived from human BLNK around the phosphorylation site of Tyr96. AA range:62-111
Specificity：Phospho-BLNK (Y96) Polyclonal Antibody detects endogenous levels of BLNK protein only when phosphorylated at Y96.
Formulation：Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source：Polyclonal, Rabbit,IgG
Dilution：WB 1:500 - 1:2000. IHC 1:100 - 1:300. ELISA: 1:20000.. IF 1:50-200
Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration：1 mg/ml
Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)
Other Name：BLNK;BASH;SLP65;B-cell linker protein;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;
Observed Band(KD)：50kD
Background： This gene encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. This protein bridges B cell receptor-associated kinase activation with downstream signaling pathways, thereby affecting various biological functions. The phosphorylation of five tyrosine residues is necessary for this protein to nucleate distinct signaling effectors following B cell receptor activation. Mutations in this gene cause hypoglobulinemia and absent B cells, a disease in which the pro- to pre-B-cell transition is developmentally blocked. Deficiency in this protein has also been shown in some cases of pre-B acute lymphoblastic leukemia. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, May 2012],
Function：disease:Defects in BLNK are the cause of hypoglobulinemia and absent B-cells [MIM:604515]. This is a developmental blockage at the pro- to pre-B-cell transition.,disease:In 6 of 34 childhood pre-B acute lymphoblastic leukemia (ALL) samples that were tested showed a complete loss or drastic reduction of BLNK expression.,function: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. 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 ac
Subcellular Location：Cytoplasm . Cell membrane . BCR activation results in the translocation to membrane fraction.
Expression：Expressed in B-cell lineage and fibroblast cell lines (at protein level). Highest levels of expression in the spleen, with lower levels in the liver, kidney, pancreas, small intestines and colon.
