• 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

• Rat Gene Id：
• 499356

• Rat Swiss Prot No：
• Q4KM52

• Immunogen：
• The antiserum was produced against synthesized peptide derived from human BLNK around the phosphorylation site of Tyr84. AA range:50-99

• Specificity：
• Phospho-BLNK (Y84) Polyclonal Antibody detects endogenous levels of BLNK protein only when phosphorylated at Y84.

• 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: 1:10000.. 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)：
• 65kD

• 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.

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