TRIM-CypA对1型人类免疫缺陷病毒的限制作用具有快速动力学特征，且独立于细胞质聚集体、泛素和蛋白酶体活性。
Restriction of human immunodeficiency virus type 1 by TRIM-CypA occurs with rapid kinetics and independently of cytoplasmic bodies, ubiquitin, and proteasome activity.
作者信息
Perez-Caballero David, Hatziioannou Theodora, Zhang Fengwen, Cowan Simone, Bieniasz Paul D
机构信息
Aaron Diamond AIDS Research Center, 455 First Avenue, New York, NY 10016, USA.
出版信息
J Virol. 2005 Dec;79(24):15567-72. doi: 10.1128/JVI.79.24.15567-15572.2005.
Abstract
TRIM-CypA is an owl monkey-specific variant of the retrovirus restriction factor TRIM5alpha. Here, we exploit its modular domain organization and cyclosporine sensitivity to probe the kinetics and mechanism of TRIM5-mediated restriction. Time of addition/withdrawal experiments reveal that inhibition of incoming human immunodeficiency virus type 1 capsids by TRIM-CypA occurs within minutes of their delivery to the target cell cytoplasm. However, while TRIM-CypA restriction is partly dependent on a RING domain, restriction occurs independently of the ubiquitin/proteasome system. Moreover, tagged TRIM-CypA proteins can be fully active as restriction factors without forming cytoplasmic bodies.
摘要
TRIM-CypA是逆转录病毒限制因子TRIM5α的一种夜猴特异性变体。在此，我们利用其模块化结构域组织和环孢菌素敏感性来探究TRIM5介导的限制作用的动力学和机制。添加/去除时间实验表明，TRIM-CypA对进入的1型人类免疫缺陷病毒衣壳的抑制作用在其被递送至靶细胞胞质后的几分钟内就会发生。然而，虽然TRIM-CypA的限制作用部分依赖于一个RING结构域，但这种限制作用的发生独立于泛素/蛋白酶体系统。此外，带有标签的TRIM-CypA蛋白可以作为限制因子完全发挥活性，而无需形成胞质体。
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