HIV-1 VPR modulates cell cycle G2/M transition through an alternative cellular mechanism other than the classic mitotic checkpoints.

摘要: HIV-1 Vpr induces cell cycle G2/M arrest in both human and fission yeast cells, suggesting a highly conserved activity of this viral protein. In review, we summarize the current understanding Vpr-induced G2 based on studies from mammalian cells (Schizosaccharomyces pombe) model system. Fission has proven to be an excellent system investigate control eukaryotic cells. Similarly, also been instrumental defining molecular mechanism underlying induced by Vpr. We have compared classic DNA-damage DNA-replication checkpoint controls transition conferred Based findings, hypothesize that through alternative novel cellular pathway(s) rather than mitotic controls. A number proteins which may involved new identified are discussed.