
人 CLIC4 抗体对
01AB01068
Chloride intracellular channel 4 (CLIC4) is a metamorphic protein that can insert into cellular membranes to form voltage-dependent, multi-ion conductive channels, with membrane insertion regulated by redox conditions and potentially occurring only under specific cellular states. Structurally, CLIC4 is related to omega-type glutathione-S-transferases (GSTs) and exhibits glutaredoxin-like enzymatic activity dependent on a conserved cysteine residue, suggesting roles beyond ion transport, such as redox regulation and signaling. CLIC4 is widely expressed across mammalian tissues and is particularly important in endothelial cells, where it promotes cell proliferation, regulates morphogenesis, and mediates cytoskeletal remodeling through RhoA signaling pathways. Functionally, CLIC4 is a critical effector in G-protein–coupled receptor signaling, notably in the sphingosine-1-phosphate (S1P) receptor pathway, and is essential for maintaining endothelial barrier integrity by modulating RhoA-mediated responses. Dysregulation of CLIC4 has been implicated in pathological processes involving endothelial dysfunction.
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技术参数
- 靶点基因名
- CLIC4
- 蛋白别名
- chloride intracellular channel 4; CLIC4
- UniProt
- Q9Y696
- 物种
- Human
产品详情
- 靶点名称
- CLIC4
- 蛋白名称
- chloride intracellular channel 4
- 蛋白别名
- Chloride intracellular channel protein 4; Intracellular chloride ion channel protein p64H1
- 靶点基因名
- CLIC4
- UniProt
- Q9Y696
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Chloride intracellular channel 4 (CLIC4) is a metamorphic protein that can insert into cellular membranes to form voltage-dependent, multi-ion conductive channels, with membrane insertion regulated by redox conditions and potentially occurring only under specific cellular states. Structurally, CLIC4 is related to omega-type glutathione-S-transferases (GSTs) and exhibits glutaredoxin-like enzymatic activity dependent on a conserved cysteine residue, suggesting roles beyond ion transport, such as redox regulation and signaling. CLIC4 is widely expressed across mammalian tissues and is particularly important in endothelial cells, where it promotes cell proliferation, regulates morphogenesis, and mediates cytoskeletal remodeling through RhoA signaling pathways. Functionally, CLIC4 is a critical effector in G-protein–coupled receptor signaling, notably in the sphingosine-1-phosphate (S1P) receptor pathway, and is essential for maintaining endothelial barrier integrity by modulating RhoA-mediated responses. Dysregulation of CLIC4 has been implicated in pathological processes involving endothelial dysfunction.