アクティブボード・２０１０年５月
　　　　　・・・・・２０１０年　５月　６日更新・・・・・

研究発表を行った学会；
17th Conference on Retroviruses and Opportunistic Infections (CROI 2010).
　２０１０年　２月１６日〜１９日（San Francisco, USA）

タイトル；Intrinsic Restriction Activity by APOBEC1 against the Mobility of Autonomous Retrotransposons.
　
発表者；　池田　輝政　氏
　　　（熊本大学　大学院生命科学研究部　感染制御分野）

Abstract；
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 (MLV) 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-to-U deamination of mRNA for apo B, has also been shown to modify a range of exogenous retroviruses, but it’s activity against endogenous retroelements remains unclear. Here we show in cell culture based retrotransposition assays that A1 family proteins can also reduce the mobility and infectivity potential of LINE-1 (long interspersed nucleotide sequence-1, L1) and long-terminal-repeats (LTR) 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 a wide range of mammalian species.