人 ADAMTS8 抗体对
01AB04205
ADAM metallopeptidase with thrombospondin type 1 motif 8 (ADAMTS8) is a member of the ADAMTS family, characterized by its metalloproteinase domain and thrombospondin motifs, which play a crucial role in extracellular matrix regulation. This enzyme is primarily expressed in the lungs and heart, where it exhibits anti-angiogenic properties and is involved in processes such as cell adhesion and proliferation. Clinically, ADAMTS8 has been associated with various diseases, notably pulmonary arterial hypertension (PAH) and several cancers, where its reduced expression may indicate a tumor suppressor role. Studies have shown that ADAMTS8 overexpression can lead to increased proliferation of pulmonary artery smooth muscle cells (PASMCs), while its deletion mitigates hypoxia-induced pulmonary hypertension, suggesting its significant involvement in vascular pathology and tumor biology.
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技术参数
- 靶点基因名
- ADAMTS8
- 基因别名
- METH2
- 蛋白别名
- ADAM metallopeptidase with thrombospondin type 1 motif 8; ADAMTS8
- UniProt
- Q9UP79
- 物种
- Human
产品详情
- 靶点名称
- ADAMTS8
- 蛋白名称
- ADAM metallopeptidase with thrombospondin type 1 motif 8
- 蛋白别名
- A disintegrin and metalloproteinase with thrombospondin motifs 8; ADAM-TS 8; ADAM-TS8; ADAMTS-8; METH-2; METH-8
- 靶点基因名
- ADAMTS8
- 基因别名
- METH2
- UniProt
- Q9UP79
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
ADAM metallopeptidase with thrombospondin type 1 motif 8 (ADAMTS8) is a member of the ADAMTS family, characterized by its metalloproteinase domain and thrombospondin motifs, which play a crucial role in extracellular matrix regulation. This enzyme is primarily expressed in the lungs and heart, where it exhibits anti-angiogenic properties and is involved in processes such as cell adhesion and proliferation. Clinically, ADAMTS8 has been associated with various diseases, notably pulmonary arterial hypertension (PAH) and several cancers, where its reduced expression may indicate a tumor suppressor role. Studies have shown that ADAMTS8 overexpression can lead to increased proliferation of pulmonary artery smooth muscle cells (PASMCs), while its deletion mitigates hypoxia-induced pulmonary hypertension, suggesting its significant involvement in vascular pathology and tumor biology.