HIV-1 entry cofactor: Functional cDNA cloning of a seven-transmembrane, G protein-coupled receptor

HIV-1 entry cofactor: Functional cDNA cloning of a seven-transmembrane, G protein-coupled receptor
复制标题

DOI:
10.1126/science.272.5263.872
复制
发表时间:
1996-05-10
期刊:
影响因子:
56.9
通讯作者:
Berger, EA
Berger, EA
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Feng, Y;Broder, CC;Berger, EA

文献摘要

被引文献

相似文献

利用一种新的功能性互补DNA(cDNA)克隆策略鉴定了HIV-1(人类免疫缺陷病毒1型)融合和进入的辅因子。这种蛋白质,命名为“融合素”,是一种假定的G蛋白偶联受体,具有七个跨膜片段。重组融合蛋白使表达CD4的非人细胞类型能够支持HIV-1 Env介导的细胞融合和HIV-1感染。融合素抗体阻断细胞融合和与正常CD4阳性人靶细胞的感染。融合信使RNA水平与不同人类细胞类型的HIV-1容许性相关。融合蛋白优先采取行动的T细胞系嗜性分离株,在与巨噬细胞嗜性HIV-1分离株的活性相比。
A cofactor for HIV-1 (human immunodeficiency virus-type 1) fusion and entry was identified with the use of a novel functional complementary DNA (cDNA) cloning strategy. This protein, designated ''fusin,'' is a putative G protein-coupled receptor with seven transmembrane segments. Recombinant fusin enabled CD4-expressing nonhuman cell types to support HIV-1 Env-mediated cell fusion and HIV-1 infection. Antibodies to fusin blocked cell fusion and infection with normal CD4-positive human target cells. Fusin messenger RNA levels correlated with HIV-1 permissiveness in diverse human cell types. Fusin acted preferentially for T cell line-tropic isolates, in comparison to its activity with macrophage-tropic HIV-1 isolates.