Footprint of APOBEC3 on the Genome of Human Retroelements (original) (raw)

“…These studies suggest that at least one aspect of the restriction mechanism does not require additional mammalian proteins as cofactors. Although most mechanistic studies have been performed in model systems, bioinformatics approaches have revealed that significant fractions of some, but not all, endogenous retroviruses have been rendered inactive by a G-to-A hypermutation mechanism, most likely mediated by A3 enzymes based on hallmark signatures (Anwar et al, 2013; Jern and Coffin, 2008; Jern et al, 2007; Lee et al, 2008). …”

Section: Apobec3 Involvement In Endogenous Virus and Transposon Restrmentioning