Persistent human Borna disease virus infection modifies the acetylome of human oligodendroglia cells towards higher energy and transporter levels.
作者： Xia Liu , Siwen Liu , Liv Bode , Chengyu Liu , Liang Zhang
DOI: 10.1016/J.VIROL.2015.06.024
关键词:
摘要: Abstract Background Borna disease virus (BDV) is a neurotropic RNA persistently infecting mammalian hosts including humans. Lysine acetylation (Kac) key protein post-translational modification (PTM). The unexpectedly broad regulatory scope of Kac let us to profile the entire acetylome upon BDV infection. Methods was profiled through stable isotope labeling for cell culture (SILAC)-based quantitative proteomics. quantifiable proteome annotated using bioinformatics. Results We identified and quantified 791 sites in 473 proteins human Hu-H1-infected non-infected oligodendroglial (OL) cells. Bioinformatic analysis revealed that infection alters metabolic proteins, membrane-associated transmembrane transporter activity, affects several lysine acetyltransferases (KAT). Conclusions Upon persistence OL manipulated towards higher energy levels necessary shuttling from nuclear replication sites.
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