| 规格 | 价格 | 库存 |
|---|---|---|
| 50ul | ¥ 1200 | 8 |
| 100ul | ¥ 1900 | 6 |
| 200ul | ¥ 2900 | 3 |
| 产品编号 | Ys-2748R |
| 英文名称 | 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. |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Mouse, (predicted: Human, Rat, Dog, Pig, Cow, Horse, Rabbit, ) |
| 产品应用 | WB=1:500-2000 ELISA=1:5000-10000 Flow-Cyt=1μg /test not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理论分子量 | 50kDa |
| 细胞定位 | 细胞浆 细胞膜 |
| 性 状 | Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human BLNK: 301-400/456 |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 缓 冲 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. |
| 注意事项 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 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: |