Deletion of the second immunoglobulin-like domain of nectin-1 alters its intracellular processing and localization and ability to mediate entry of herpes simplex virus.
Deletion of the second immunoglobulin-like domain of nectin-1 alters its intracellular processing and localization and ability to mediate entry of herpes simplex virus.
复制标题
nectin-1 的第二个免疫球蛋白样结构域的缺失会改变其细胞内加工和定位以及介导单纯疱疹病毒进入的能力。
DOI：
10.1128/jvi.79.6.3841-3845.2005
复制
发表时间：
2005
影响因子：
5.4
通讯作者：
Spear,PatriciaG
中科院分区：
文献类型：
--
作者：
Struyf,Frank;Plate,AileenE;Spear,PatriciaG
Nectin-1是单纯疱疹病毒(HSV)免疫球蛋白(Ig)样进入受体。与其他果胶一样，果胶-1形成二聚体，并通过与其他果胶的相互作用调节细胞黏附。我们构建了Nectin-1的第二结构域缺失突变体(Nectin-1-Δ2)，以研究第二Ig样结构域在HSV进入中的作用。Nectin-1-Δ-2介导单纯疱疹病毒进入的能力显著降低，并聚集在内质网中，但保留了与其配体Gd相互作用的能力。Nectin-1-Δ2不能介导单纯疱疹病毒的进入可能是由于它不能被转运到单纯疱疹病毒靶向的膜上而导致的。
Nectin-1 is an immunoglobulin (Ig)-like entry receptor for herpes simplex virus (HSV). Like other nectins, nectin-1 forms dimers and mediates cell adhesion through interactions with other nectins. We constructed a second-domain deletion mutant of nectin-1 (nectin-1-Δ2) to examine the role of the second Ig-like domain in HSV entry. Nectin-1-Δ2 exhibited a severely reduced ability to mediate HSV entry and accumulated in the endoplasmic reticulum but retained the ability to interact with its HSV ligand, gD. The failure of nectin-1-Δ2 to mediate HSV entry probably resulted from its failure to be transported to a membrane targeted by HSV for viral entry.