人 CX3CL1 抗体对
01AB01676
C-X3-C motif chemokine ligand 1 (CX3CL1) is a unique CX3C-type chemokine synthesized as a type I transmembrane glycoprotein. It features a chemokine domain positioned on an extended mucin-like stalk, followed by a transmembrane segment and a short cytoplasmic tail. The membrane-bound form mediates the firm, integrin-independent adhesion of leukocytes to activated endothelium. Proteolytic shedding by metalloproteases, such as ADAM10 and ADAM17, releases a soluble form that acts as a potent chemoattractant for T cells and monocytes via its receptor, CX3CR1. This signaling axis activates MAPK/AKT pathways and regulates leukocyte trafficking, neuroglial communication, and synaptic plasticity. Clinically, dysregulation of CX3CL1 is associated with atherosclerosis, vasculitis, and neurodegenerative diseases. In oncology, it influences the immune microenvironment and can promote tumor cell proliferation, migration, and resistance to apoptosis in a context-dependent manner.
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技术参数
- 靶点基因名
- CX3CL1
- 基因别名
- FKN; NTT; SCYD1
- 蛋白别名
- C-X3-C motif chemokine ligand 1; CX3CL1
- UniProt
- P78423
- 物种
- Human
产品详情
- 靶点名称
- CX3CL1
- 蛋白名称
- C-X3-C motif chemokine ligand 1
- 蛋白别名
- Fractalkine; C-X3-C motif chemokine 1; CX3C membrane-anchored chemokine; Neurotactin; Small-inducible cytokine D1) [Cleaved into: Processed fractalkine]
- 靶点基因名
- CX3CL1
- 基因别名
- FKN; NTT; SCYD1
- UniProt
- P78423
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
C-X3-C motif chemokine ligand 1 (CX3CL1) is a unique CX3C-type chemokine synthesized as a type I transmembrane glycoprotein. It features a chemokine domain positioned on an extended mucin-like stalk, followed by a transmembrane segment and a short cytoplasmic tail. The membrane-bound form mediates the firm, integrin-independent adhesion of leukocytes to activated endothelium. Proteolytic shedding by metalloproteases, such as ADAM10 and ADAM17, releases a soluble form that acts as a potent chemoattractant for T cells and monocytes via its receptor, CX3CR1. This signaling axis activates MAPK/AKT pathways and regulates leukocyte trafficking, neuroglial communication, and synaptic plasticity. Clinically, dysregulation of CX3CL1 is associated with atherosclerosis, vasculitis, and neurodegenerative diseases. In oncology, it influences the immune microenvironment and can promote tumor cell proliferation, migration, and resistance to apoptosis in a context-dependent manner.