Langlois Marc-André, Neuberger Michael S
Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, United Kingdom.
J Virol. 2008 May;82(9):4660-4. doi: 10.1128/JVI.02469-07. Epub 2008 Feb 13.
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.
载脂蛋白B mRNA编辑酶催化多肽样蛋白3（APOBEC3）家族蛋白是哺乳动物特有的胞苷脱氨酶，能够限制逆转录病毒感染。这种限制的确切机制尚未明确，但有一种模型认为，由胞苷脱氨基作用产生的尿嘧啶化逆转录病毒cDNA是细胞糖基化酶的作用靶点。虽然UNG缺陷并不影响这种限制作用，但有研究表明，SMUG1糖基化酶可能起到了备用作用。我们发现，将人类APOBEC3G导入鸡细胞中可实现逆转录病毒限制（这与APOBEC3介导的限制作用所需成分早于哺乳动物进化的观点一致），并利用该实验证明，在UNG和SMUG1均缺陷的细胞中也可发生APOBEC3G介导的限制作用。
