HIV组装和出芽:Ca(2+)信号和非escrt蛋白设置阶段。

Molecular biology international Pub Date : 2012-01-01 Epub Date: 2012-06-12 DOI:10.1155/2012/851670
Lorna S Ehrlich, Carol A Carter
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引用次数: 15

摘要

自从首次发现运输所需的内体分选复合体(ESCRT)机制与HIV-1蛋白运输和出芽之间的联系以来,已经过去了十多年。HIV-1 Gag中的L结构域介导ESCRT的募集,ESCRT在芽脱落中起作用,将病毒颗粒从宿主细胞中释放出来。除了病毒出芽,ESCRT机制还参与内吞途径、细胞分裂和自噬。在过去的几年中,非escrt宿主蛋白在组装过程中所必需的数量也有所增加。在本文中,我们强调了最近发现的将ESCRT机制与钙信号机制联系起来的细胞因子的作用,我们认为这种联系有助于为ESCRT的有效募集和脱落调解奠定基础。将讨论非escrt在病毒出芽和细胞分裂中的平行作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

HIV Assembly and Budding: Ca(2+) Signaling and Non-ESCRT Proteins Set the Stage.

HIV Assembly and Budding: Ca(2+) Signaling and Non-ESCRT Proteins Set the Stage.

HIV Assembly and Budding: Ca(2+) Signaling and Non-ESCRT Proteins Set the Stage.

HIV Assembly and Budding: Ca(2+) Signaling and Non-ESCRT Proteins Set the Stage.

More than a decade has elapsed since the link between the endosomal sorting complex required for transport (ESCRT) machinery and HIV-1 protein trafficking and budding was first identified. L domains in HIV-1 Gag mediate recruitment of ESCRT which function in bud abscission releasing the viral particle from the host cell. Beyond virus budding, the ESCRT machinery is also involved in the endocytic pathway, cytokinesis, and autophagy. In the past few years, the number of non-ESCRT host proteins shown to be required in the assembly process has also grown. In this paper, we highlight the role of recently identified cellular factors that link ESCRT machinery to calcium signaling machinery and we suggest that this liaison contributes to setting the stage for productive ESCRT recruitment and mediation of abscission. Parallel paradigms for non-ESCRT roles in virus budding and cytokinesis will be discussed.

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