Human APOBEC3G can restrict retroviral infection in avian cells and acts independently of both UNG and SMUG1
Human APOBEC3G can restrict retroviral infection in avian cells and acts independently of both UNG and SMUG1
复制标题
DOI：
10.1128/jvi.02469-07
复制
发表时间：
2008-05-01
影响因子：
5.4
通讯作者：
Neuberger, Michael S.
中科院分区：
文献类型：
--
作者：
Langlois, Marc-Andre;Neuberger, Michael S.
APOBEC3蛋白是哺乳动物特异性胞苷脱氨酶，可以限制逆转录病毒感染。限制的确切机制尚未解决，但一种模型设想，尿嘧啶化的逆转录病毒cDNA，由胞苷脱氨基作用产生，是细胞糖基化酶的目标。虽然限制不受UNG缺陷的影响，但已表明SMUG1糖基化酶可能提供备份。我们发现，逆转录病毒限制可以通过将人APOBEC3G引入鸡细胞（与APOBEC3介导的限制先于哺乳动物进化所必需的成分一致）来实现，并使用该试验表明，APOBEC3G介导的限制可以发生在UNG和SMUG1缺陷的细胞中。
APOBEC3 proteins are mammal-specific cytidine deaminases that can restrict retroviral infection. The exact mechanism of the restriction remains unresolved, but one model envisions that uracilated retroviral cDNA, generated by cytidine deamination, is the target of cellular glycosylases. While restriction is unaffected by UNG deficiency, it has been suggested that the SMUG1 glycosylase might provide a backup. We found that retroviral restriction can be achieved by introducing human APOBEC3G into chicken cells (consistent with the components necessary for APOBEC3-mediated restriction predating mammalian evolution) and used this assay to show that APOBEC3G-mediated restriction can occur in cells deficient in both UNG and SMUG1.