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ACKR3 (基因名), Atypical chemokine receptor 3 (蛋白名), ACKR3_CANLF.
产品名称:

Dog ACKR3/ Atypical chemokine receptor 3 ELISA Kit

货号:
-
商标:
EIAab®
监管等级:
别名:

C-X-C chemokine receptor type 7, Chemokine orphan receptor 1, G-protein coupled receptor RDC1, CXC-R7, RDC-1, CMKOR1, CXCR7, RDC1

检测方法:
ELISA
特异性:
Natural and recombinant dog Atypical chemokine receptor 3
样品类型:
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
样品数据:
研究领域:
-
Dog ACKR3 ELISA Kit
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Dog ACKR3 ELISA Kit
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产品说明书
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通用注释


亚单元:
Homodimer. Can form heterodimers with CXCR4; heterodimerization may regulate CXCR4 signaling activity (By similarity). Interacts with ARRB1 and ARRB2.


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 CXCL11 and CXCL12/SDF1. Chemokine binding does not activate G-protein-mediated signal transduction but instead induces beta-arrestin recruitment, leading to ligand internalization and activation of MAPK signaling pathway. Required for regulation of CXCR4 protein levels in migrating interneurons, thereby adapting their chemokine responsiveness. In glioma cells, transduces signals via MEK/ERK pathway, mediating resistance to apoptosis. Promotes cell growth and survival. Not involved in cell migration, adhesion or proliferation of normal hematopoietic progenitors but activated by CXCL11 in malignant hemapoietic cells, leading to phosphorylation of ERK1/2 (MAPK3/MAPK1) and enhanced cell adhesion and migration. Plays a regulatory role in CXCR4-mediated activation of cell surface integrins by CXCL12. Required for heart valve development.


亚细胞位置:
Cell membrane Multi-pass membrane protein Cytoplasm Perinuclear region Early endosome Recycling endosome Predominantly localizes to endocytic vesicles, and upon stimulation by the ligand is internalized via clathrin-coated pits in a beta-arrestin-dependent manner. 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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