Ackr2 (基因名), Atypical chemokine receptor 2 (蛋白名), ackr2_mouse.
产品名称:
Mouse Ackr2/ Atypical chemokine receptor 2 CLIA Kit
非典型趋化因子受体2
货号:
U14064m
商标:
EIAab®
监管等级:
别名:
C-C chemokine receptor D6, Chemokine-binding protein 2, Chemokine-binding protein D6, Ccbp2, D6
检测方法:
CLIA
特异性:
Natural and recombinant mouse Atypical chemokine receptor 2
样品类型:
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
样品数据:
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研究领域:
-
通用注释
亚单元:
N/A
功能:
Atypical chemokine receptor that controls chemokine levels and localization via high-affinity chemokine binding that is uncoupled from classic ligand-driven signal transduction cascades, resulting instead in chemokine sequestration, degradation, or transcytosis. Also known as interceptor (internalizing receptor) or chemokine-scavenging receptor or chemokine decoy receptor. Acts as a receptor for chemokines including CCL2, CCL3, CCL3L1, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL17, CCL22, CCL23, CCL24, SCYA2/MCP-1, SCY3/MIP-1-alpha, SCYA5/RANTES and SCYA7/MCP-3. Upon active ligand stimulation, activates a beta-arrestin 1 (ARRB1)-dependent, G protein-independent signaling pathway that results in the phosphorylation of the actin-binding protein cofilin (CFL1) through a RAC1-PAK1-LIMK1 signaling pathway. Activation of this pathway results in up-regulation of ACKR2 from endosomal compartment to cell membrane, increasing its efficiency in chemokine uptake and degradation. By scavenging chemokines in tissues, on the surfaces of lymphatic vessels, and in placenta, plays an essential role in the resolution (termination) of the inflammatory response and in the regulation of adaptive immune responses. Plays a major role in the immune silencing of macrophages during the resolution of inflammation. Acts as a regulator of inflammatory leukocyte interactions with lymphatic endothelial cells (LECs) and is required for immature/mature dendritic cells discrimination by LECs.
亚细胞位置:
Early endosome
Recycling endosome
Cell membrane
Multi-pass membrane protein
Predominantly localizes to endocytic vesicles, and upon stimulation by the ligand is internalized via clathrin-coated pits. Once internalized, the ligand dissociates from the receptor, and is targeted to degradation while the receptor is recycled back to the cell membrane (By similarity).
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