人 BLNK 抗体对
01AB00458
B cell linker (BLNK), also known as SLP-65, BASH, and BCA, is a cytoplasmic adaptor protein crucial for B cell development and receptor signaling. It lacks intrinsic enzymatic activity but plays a pivotal role in coordinating and regulating downstream signaling effectors in B cell receptor (BCR) signaling. BLNK consists of a N-terminal leucine zipper motif, an acidic region, a proline-rich region, and a C-terminal SH2 domain, which allows it to localize to the plasma membrane and interact with various signaling proteins. Phosphorylation of BLNK by Syk tyrosine kinase provides docking sites for SH2-containing effector molecules such as Grb2, PLCγ2, Btk, Vav, and Nck, facilitating the activation of their respective signaling pathways. Deficiency in BLNK leads to impaired B cell development, with knockout mice showing a partial block and humans exhibiting a more profound block in B cell development. Additionally, BLNK may have tumor suppressive activity through its interaction with Bruton's tyrosine kinase (Btk) and regulation of the pre-B cell checkpoint.
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技术参数
- 靶点基因名
- BLNK
- 基因别名
- BASH; SLP65
- 蛋白别名
- B cell linker; BLNK
- UniProt
- Q8WV28
- 物种
- Human
产品详情
- 靶点名称
- BLNK
- 蛋白名称
- B cell linker
- 蛋白别名
- 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; SLP-65
- 靶点基因名
- BLNK
- 基因别名
- BASH; SLP65
- UniProt
- Q8WV28
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
B cell linker (BLNK), also known as SLP-65, BASH, and BCA, is a cytoplasmic adaptor protein crucial for B cell development and receptor signaling. It lacks intrinsic enzymatic activity but plays a pivotal role in coordinating and regulating downstream signaling effectors in B cell receptor (BCR) signaling. BLNK consists of a N-terminal leucine zipper motif, an acidic region, a proline-rich region, and a C-terminal SH2 domain, which allows it to localize to the plasma membrane and interact with various signaling proteins. Phosphorylation of BLNK by Syk tyrosine kinase provides docking sites for SH2-containing effector molecules such as Grb2, PLCγ2, Btk, Vav, and Nck, facilitating the activation of their respective signaling pathways. Deficiency in BLNK leads to impaired B cell development, with knockout mice showing a partial block and humans exhibiting a more profound block in B cell development. Additionally, BLNK may have tumor suppressive activity through its interaction with Bruton's tyrosine kinase (Btk) and regulation of the pre-B cell checkpoint.