人 VASH1 抗体对
01AB01615
Vasohibin 1 (VASH1) is primarily expressed in endothelial cells (ECs) and composed of 365 amino acids in its main isoform. It functions as a negative feedback regulator of angiogenesis, being induced by angiogenic factors such as VEGF and FGF-2, and acts to inhibit endothelial cell migration and network formation, thereby terminating new blood vessel formation. Unlike many angiogenesis inhibitors that promote EC death, VASH1 uniquely enhances EC survival under stress by upregulating antioxidant enzymes like superoxide dismutase 2 and anti-aging proteins such as SIRT1, which increases resistance to oxidative stress and cellular aging. VASH1 also forms a detyrosinating enzyme complex with SVBP, contributing to microtubule regulation in nonmuscle cells and affecting cardiomyocyte mechanics. Clinically, VASH1’s role as an angiogenesis inhibitor has implications in pathological conditions such as cancer, where its expression can suppress tumor vascularization, and in cardiovascular diseases, where its modulation influences heart muscle cell function and may impact heart failure progression.
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技术参数
- 靶点基因名
- VASH1
- 基因别名
- KIAA1036; VASH
- 蛋白别名
- vasohibin 1; VASH1
- UniProt
- Q7L8A9
- 物种
- Human
产品详情
- 靶点名称
- VASH1
- 蛋白名称
- vasohibin 1
- 蛋白别名
- Tubulinyl-Tyr carboxypeptidase 1; Tubulin carboxypeptidase 1; Tyrosine carboxypeptidase 1; TTCP 1; Vasohibin-1
- 靶点基因名
- VASH1
- 基因别名
- KIAA1036; VASH
- UniProt
- Q7L8A9
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Vasohibin 1 (VASH1) is primarily expressed in endothelial cells (ECs) and composed of 365 amino acids in its main isoform. It functions as a negative feedback regulator of angiogenesis, being induced by angiogenic factors such as VEGF and FGF-2, and acts to inhibit endothelial cell migration and network formation, thereby terminating new blood vessel formation. Unlike many angiogenesis inhibitors that promote EC death, VASH1 uniquely enhances EC survival under stress by upregulating antioxidant enzymes like superoxide dismutase 2 and anti-aging proteins such as SIRT1, which increases resistance to oxidative stress and cellular aging. VASH1 also forms a detyrosinating enzyme complex with SVBP, contributing to microtubule regulation in nonmuscle cells and affecting cardiomyocyte mechanics. Clinically, VASH1’s role as an angiogenesis inhibitor has implications in pathological conditions such as cancer, where its expression can suppress tumor vascularization, and in cardiovascular diseases, where its modulation influences heart muscle cell function and may impact heart failure progression.