抗人 SCIN 抗体对
01AB01584
Scinderin (SCIN), also known as adseverin, is a calcium-dependent actin-severing and capping protein belonging to the gelsolin superfamily, predominantly expressed in secretory tissues where it regulates cortical actin networks and facilitates vesicle movement during secretion by severing actin filaments in response to increased intracellular calcium. SCIN plays a critical role in actin cytoskeletal organization, osteoclastogenesis, and the regulation of chondrocyte proliferation and differentiation, influencing cellular processes such as cell proliferation and differentiation through pathways involving MAPK and p38 signaling. Functionally, SCIN inhibits cell proliferation and tumorigenesis, and its overexpression has been shown to downregulate cyclin A1 and phosphorylated STAT3, thereby promoting cell cycle arrest at the S/G2 phase and suppressing oncogenic signaling. Clinically, altered SCIN expression is associated with various cancers, where reduced SCIN levels can predict poor prognosis and increased tumor cell proliferation.
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技术参数
- 靶点基因名
- SCIN
- 基因别名
- KIAA1905
- 蛋白别名
- scinderin; SCIN
- UniProt
- Q9Y6U3
- 物种
- Human
产品详情
- 靶点名称
- SCIN
- 蛋白名称
- scinderin
- 蛋白别名
- Scinderin; Adseverin
- 靶点基因名
- SCIN
- 基因别名
- KIAA1905
- UniProt
- Q9Y6U3
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Scinderin (SCIN), also known as adseverin, is a calcium-dependent actin-severing and capping protein belonging to the gelsolin superfamily, predominantly expressed in secretory tissues where it regulates cortical actin networks and facilitates vesicle movement during secretion by severing actin filaments in response to increased intracellular calcium. SCIN plays a critical role in actin cytoskeletal organization, osteoclastogenesis, and the regulation of chondrocyte proliferation and differentiation, influencing cellular processes such as cell proliferation and differentiation through pathways involving MAPK and p38 signaling. Functionally, SCIN inhibits cell proliferation and tumorigenesis, and its overexpression has been shown to downregulate cyclin A1 and phosphorylated STAT3, thereby promoting cell cycle arrest at the S/G2 phase and suppressing oncogenic signaling. Clinically, altered SCIN expression is associated with various cancers, where reduced SCIN levels can predict poor prognosis and increased tumor cell proliferation.