载脂蛋白B mRNA编辑酶催化多肽1（APOBEC-1）和激活诱导胞嘧啶脱氨酶（AID）是核质运输蛋白，但载脂蛋白B mRNA编辑酶催化多肽3G（APOBEC3G）无法进行运输。
APOBEC-1 and AID are nucleo-cytoplasmic trafficking proteins but APOBEC3G cannot traffic.
作者信息
Bennett Ryan P, Diner Elie, Sowden Mark P, Lees Joshua A, Wedekind Joseph E, Smith Harold C
机构信息
Department of Biochemistry, Box 712, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.
出版信息
Biochem Biophys Res Commun. 2006 Nov 10;350(1):214-9. doi: 10.1016/j.bbrc.2006.09.032. Epub 2006 Sep 18.
Abstract
Human APOBEC3G (hA3G) is a member of the APOBEC-1 related protein (ARP) family of cytidine deaminases. hA3G functions as a natural defense against endogenous retrotransposons and a multitude of retroviruses, most notably human immunodeficiency virus type 1 (HIV-1). Nothing is known about the cellular function of hA3G, however, upon HIV-1 infection hA3G functions as an antiviral factor by mutating viral single-stranded DNA during reverse transcription. Whereas homologous deaminases such as APOBEC-1 and AID act on RNA and DNA, respectively, in the cell nucleus, hA3G mutagenic activity appears to be restricted to the cytoplasm. We demonstrate that hA3G is not a nucleo-cytoplasmic shuttling protein like APOBEC-1 and AID, but is strongly retained in the cytoplasm through a mechanism that involves both the N and C-terminal regions of the protein.
摘要
人类载脂蛋白B mRNA编辑酶催化多肽样蛋白3G（hA3G）是胞苷脱氨酶中与载脂蛋白B mRNA编辑酶催化多肽样蛋白1相关蛋白（ARP）家族的成员。hA3G作为一种天然防御机制，可抵御内源性逆转录转座子和多种逆转录病毒，其中最显著的是1型人类免疫缺陷病毒（HIV-1）。然而，关于hA3G的细胞功能尚无定论，不过在HIV-1感染时，hA3G通过在逆转录过程中使病毒单链DNA发生突变，发挥抗病毒因子的作用。虽然同源脱氨酶如载脂蛋白B mRNA编辑酶催化多肽样蛋白1和活化诱导胞嘧啶脱氨酶分别在细胞核中作用于RNA和DNA，但hA3G的诱变活性似乎局限于细胞质。我们证明，hA3G不像载脂蛋白B mRNA编辑酶催化多肽样蛋白1和活化诱导胞嘧啶脱氨酶那样是一种穿梭于核质之间的蛋白，而是通过一种涉及该蛋白N端和C端区域的机制，被强烈地保留在细胞质中。
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