Intrinsic restriction activity by apolipoprotein B mRNA editing enzyme APOBEC1 against the mobility of autonomous retrotransposons.
Intrinsic restriction activity by apolipoprotein B mRNA editing enzyme APOBEC1 against the mobility of autonomous retrotransposons.
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DOI:
10.1093/nar/gkr124
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发表时间:
2011-07
影响因子:
14.9
通讯作者:
Koito A
中科院分区:
文献类型:
--
作者:
Ikeda T;Abd El Galil KH;Tokunaga K;Maeda K;Sata T;Sakaguchi N;Heidmann T;Koito A
The ability of mammalian cytidine deaminases encoded by the APOBEC3 (A3) genes to restrict a broad number of endogenous retroelements and exogenous retroviruses, including murine leukemia virus and human immunodeficiency virus (HIV)-1, is now well established. The RNA editing family member apolipoprotein B (apo B)-editing catalytic subunit 1 (APOBEC1; A1) from a variety of mammalian species, a protein involved in lipid transport and which mediates C–U deamination of mRNA for apo B, has also been shown to modify a range of exogenous retroviruses, but its activity against endogenous retroelements remains unclear. Here, we show in cell culture-based retrotransposition assays that A1 family proteins from multiple mammalian species can also reduce the mobility and infectivity potential of LINE-1 (long interspersed nucleotide sequence-1, L1) and long-terminal repeats (LTRs) retrotransposons (or endogenous retroviruses), such as murine intracisternal A-particle (IAP) and MusD sequences. The anti-L1 activity of A1 was mainly mediated by a deamination-independent mechanism, and was not affected by subcellular localization of the proteins. In contrast, the inhibition of LTR-retrotransposons appeared to require the deaminase activity of A1 proteins. Thus, the AID/APOBEC family proteins including A1s employ multiple mechanisms to regulate the mobility of autonomous retrotransposons in several mammalian species.
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DOI:
10.1073/pnas.0831042100
发表时间:
2003-04-29
影响因子:
11.1
作者:
Brouha, B;Schustak, J;Kazazian, HH
通讯作者:
Kazazian, HH
影响因子:
14.9
作者:
Esnault, C;Casella, JF;Heidmann, T
通讯作者:
Heidmann, T
影响因子:
9.8
作者:
Brouha, B;Meischl, C;Kazazian, HH
通讯作者:
Kazazian, HH
影响因子:
56.9
作者:
Bishop, KN;Holmes, RK;Malim, MH
通讯作者:
Malim, MH
影响因子:
64.8
作者:
Esnault, C;Heidmann, O;Schwartz, O
通讯作者:
Schwartz, O