Combadiere C, Ahuja S K, Tiffany H L, Murphy P M
The Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
J Leukoc Biol. 1996 Jul;60(1):147-52. doi: 10.1002/jlb.60.1.147.
We have cloned a human cDNA for a novel CC chemokine receptor (CC CKR) designated CC CKR5 that has 48-75% amino acid identity to other CC CKRs. CC CKR5 mRNA was detected constitutively in primary adherent monocytes but not in primary neutrophils or eosinophils. Macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and RANTES were all potent agonists for CC CKR5 (EC50 = 3-30 nM) when calcium flux was measured in transfected HEK 293 cells, yet the apparent binding affinities of the corresponding iodinated chemokines to intact cells expressing the receptor were low (IC50 approximately 100 nM). The calcium flux responses were completely blocked by treatment of transfected cells with pertussis toxin. These data suggest that CC CKR5 is a G(i)-coupled receptor that may mediate monocyte responses to MIP-1alpha, MIP-1beta, and RANTES.
我们克隆了一种新型CC趋化因子受体（CC CKR）的人cDNA，命名为CC CKR5，它与其他CC CKRs具有48 - 75%的氨基酸同一性。在原代贴壁单核细胞中可组成性检测到CC CKR5 mRNA，但在原代中性粒细胞或嗜酸性粒细胞中未检测到。当在转染的HEK 293细胞中测量钙流时，巨噬细胞炎性蛋白-1α（MIP-1α）、MIP-1β和RANTES都是CC CKR5的有效激动剂（EC50 = 3 - 30 nM），然而相应的碘化趋化因子与表达该受体的完整细胞的表观结合亲和力较低（IC50约为100 nM）。用百日咳毒素处理转染细胞可完全阻断钙流反应。这些数据表明CC CKR5是一种G(i)偶联受体，可能介导单核细胞对MIP-1α、MIP-1β和RANTES的反应。
