抗人 NOTCH3 抗体对
01AB03317
Notch receptor 3 (NOTCH3) is a single-pass type I transmembrane receptor that mediates juxtacrine signaling to control cell fate, differentiation, and survival, particularly within vascular smooth muscle cells. Upon binding to membrane-bound ligands such as Jagged or Delta-like proteins, the receptor undergoes proteolytic cleavage to release its intracellular domain. This domain translocates to the nucleus and forms a transcriptional complex with RBPJ to regulate target gene expression. NOTCH3 is essential for vascular integrity and is highly expressed in tissues such as the placenta and adipose tissue. Clinically, mutations in the EGF-like repeats of NOTCH3 are the definitive cause of CADASIL, an autosomal dominant small-vessel arteriopathy characterized by recurrent strokes and leukoencephalopathy. Gain-of-function mutations are also linked to lateral meningocele syndrome.
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技术参数
- 靶点基因名
- NOTCH3
- 蛋白别名
- notch receptor 3; NOTCH3
- UniProt
- Q9UM47
- 物种
- Human
产品详情
- 靶点名称
- NOTCH3
- 蛋白名称
- notch receptor 3
- 蛋白别名
- Neurogenic locus notch homolog protein 3; Notch 3) [Cleaved into: Notch 3 extracellular truncation; Notch 3 intracellular domain]
- 靶点基因名
- NOTCH3
- UniProt
- Q9UM47
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Notch receptor 3 (NOTCH3) is a single-pass type I transmembrane receptor that mediates juxtacrine signaling to control cell fate, differentiation, and survival, particularly within vascular smooth muscle cells. Upon binding to membrane-bound ligands such as Jagged or Delta-like proteins, the receptor undergoes proteolytic cleavage to release its intracellular domain. This domain translocates to the nucleus and forms a transcriptional complex with RBPJ to regulate target gene expression. NOTCH3 is essential for vascular integrity and is highly expressed in tissues such as the placenta and adipose tissue. Clinically, mutations in the EGF-like repeats of NOTCH3 are the definitive cause of CADASIL, an autosomal dominant small-vessel arteriopathy characterized by recurrent strokes and leukoencephalopathy. Gain-of-function mutations are also linked to lateral meningocele syndrome.