The Mechanism of Budding of Retroviruses From Cell Membranes.

The Mechanism of Budding of Retroviruses From Cell Membranes.
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DOI:
10.1155/2009/623969
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发表时间:
2009-01-01
影响因子:
2.2
通讯作者:
Leis J
Leis J
中科院分区:
其他
文献类型:
--
作者:
Pincetic A;Leis J

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逆转录病毒已经进化出一种从细胞膜释放颗粒的机制,该机制适合细胞蛋白复合物,称为 ESCRT-I、-II、-III,通常参与多泡体的生物发生。 Gag 中编码的三种不同类别的晚期组装 (L) 结构域(核心序列为 PPXY、PTAP 和 YPXL)招募 ESCRT 机制的不同组件,形成用于病毒释放的出芽复合体。在这里,我们重点介绍了在确定不同 ESCRT 复合物在促进禽肉瘤和白血病病毒 (ASLV) 和 1 型人类免疫缺陷病毒 (HIV-1) 出芽、泛素化和膜靶向方面的作用方面的最新进展。这些发现表明,逆转录病毒可能通过从常见的细胞机制中招募不同的宿主因子来释放颗粒,从而采用平行的出芽途径。
Retroviruses have evolved a mechanism for the release of particles from the cell membrane that appropriates cellular protein complexes, referred to as ESCRT-I, -II, -III, normally involved in the biogenesis of multivesicular bodies. Three different classes of late assembly (L) domains encoded in Gag, with core sequences of PPXY, PTAP, and YPXL, recruit different components of the ESCRT machinery to form a budding complex for virus release. Here, we highlight recent progress in identifying the role of different ESCRT complexes in facilitating budding, ubiquitination, and membrane targeting of avian sarcoma and leukosis virus (ASLV) and human immunodeficiency virus, type 1 (HIV-1). These findings show that retroviruses may adopt parallel budding pathways by recruiting different host factors from common cellular machinery for particle release.
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