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人 CLIC4 抗体对
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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.

Human
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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.