B淋巴细胞连接蛋白抗体

B淋巴细胞连接蛋白抗体英文名称  Anti-BLNK 

中文名称  B淋巴细胞连接蛋白抗体 

别    名  B cell adapter containing SH2 domain protein; B cell adapter containing Src homology 2 domain protein; B cell linker; B cell linker protein; B cell linker protein; B-cell adapter containing a SH2 domain protein; B-cell adapter containing a Src homology 2 domain protein; B-cell linker protein; BASH; BASH; Bca; Bca; BLNK; BLNK s; BLNK_HUMAN; Cytoplasmic adapter protein; Ly 57; Ly-57; Ly57; Lymphocyte antigen 57; Lymphocyte antigen-57; Lyw 57; Lyw-57; Lyw57; MGC111051; SLP 65; SLP65; SLP-65; Src homology 2 domain containing leukocyte protein of 65 kDa. 

浓    度  1mg/1ml 

规 格  0.1ml/100μg  0.2ml/200μg   

抗体来源  Rabbit  

克隆类型  polyclonal 

交叉反应  Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit   

产品类型  一抗    

研究领域  免疫学 信号转导 细胞粘附分子 细胞表面分子 b-淋巴细胞  

蛋白分子量  predicted molecular weight: 65kDa 

性    状  Lyophilized or Liquid 

免 疫 原  KLH conjugated synthetic peptide derived from human BLNK C-terminus 

亚    型  IgG 

纯化方法  affinity purified by Protein A 

储 存 液  0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide 

产品应用   WB=1:100-500  ELISA=1:500-1000  IP=1:20-100  IHC-P=1:100-500  IHC-F=1:100-500  IF=1:100-500 

（石蜡切片需做抗原修复） 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存条件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

B淋巴细胞连接蛋白抗体产品介绍 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 : 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 activation of MAP kinase and phosphatidyl-inositol 3 (PI3) kinase signaling. May be required for the RAC1-JNK pathway. Plays a critical role in orchestrating the pro-B cell to pre-B cell transition (By similarity). Plays an important role in BCR-induced B-cell apoptosis.

Subunit : Associates with PLCG1, VAV1 and NCK1 in a B-cell antigen receptor-dependent fashion. Interacts with VAV3, PLCG2 and GRB2. Interacts through its SH2 domain with CD79A.

Subcellular Location : Cytoplasm. Cell membrane. BCR activation results in the translocation to membrane fraction.

Tissue Specificity : 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.

Post-translational modifications : Following BCR activation, phosphorylated on tyrosine residues by SYK and LYN. When phosphorylated, serves as a scaffold to assemble downstream targets of antigen activation, including PLCG1, VAV1, GRB2 and NCK1. Phosphorylation of Tyr-84, Tyr-178 and Tyr-189 facilitates PLCG1 binding. Phosphorylation of Tyr-96 facilitates BTK binding. Phosphorylation of Tyr-72 facilitates VAV1 and NCK1 binding. Phosphorylation is required for both Ca(2+) and MAPK signaling pathways.

DISEASE : Defects in BLNK are the cause of agammaglobulinemia type 4 (AGM4) [MIM:613502]. It 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. Affected individuals develop severe infections in the first years of life.

Similarity : Contains 1 SH2 domain.

Database links : UniProtKB/Swiss-Prot: Q8WV28.2