人 S100A16 抗体对
01AB02892
S100 calcium binding protein A16 (S100A16) is a small acidic cytoplasmic protein of the S100 family characterized by EF-hand calcium-binding motifs. It functions as a homodimer in calcium-dependent signaling pathways, participating in cell proliferation, migration, and epithelial-mesenchymal transition (EMT). S100A16 often exerts its effects by regulating the ubiquitin-mediated degradation of target proteins, such as LATS1 and ZO-2. Clinically, S100A16 is consistently upregulated in various malignancies, including glioma and gastric cancer, where high expression correlates with poor prognosis. In glioma, it promotes invasion by enhancing CUL4A-mediated degradation of LATS1, thereby inhibiting Hippo signaling and increasing nuclear YAP activity. In gastric cancer, it drives metastasis and EMT by promoting the degradation of the tight junction protein ZO-2, facilitating tumor spread.
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技术参数
- 靶点基因名
- S100A16
- 基因别名
- S100F
- 蛋白别名
- S100 calcium binding protein A16; S100A16
- UniProt
- Q96FQ6
- 物种
- Human
产品详情
- 靶点名称
- S100A16
- 蛋白名称
- S100 calcium binding protein A16
- 蛋白别名
- Protein S100-A16; Aging-associated gene 13 protein; Protein S100-F; S100 calcium-binding protein A16
- 靶点基因名
- S100A16
- 基因别名
- S100F
- UniProt
- Q96FQ6
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
S100 calcium binding protein A16 (S100A16) is a small acidic cytoplasmic protein of the S100 family characterized by EF-hand calcium-binding motifs. It functions as a homodimer in calcium-dependent signaling pathways, participating in cell proliferation, migration, and epithelial-mesenchymal transition (EMT). S100A16 often exerts its effects by regulating the ubiquitin-mediated degradation of target proteins, such as LATS1 and ZO-2. Clinically, S100A16 is consistently upregulated in various malignancies, including glioma and gastric cancer, where high expression correlates with poor prognosis. In glioma, it promotes invasion by enhancing CUL4A-mediated degradation of LATS1, thereby inhibiting Hippo signaling and increasing nuclear YAP activity. In gastric cancer, it drives metastasis and EMT by promoting the degradation of the tight junction protein ZO-2, facilitating tumor spread.