ArticleVirology journal2011
Human immunodeficiency virus type 1 Vif causes dysfunction of Cdk1 and CyclinB1: implications for cell cycle arrest.
Article in Virology journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- HIV-1 Vif disrupts phosphatase feedback regulation at the kinetochore, leading to a pronounced pseudo-metaphase arrest.bioRxiv : the preprint server for biology · 2024Article
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Biomedical association analysis between G2/M checkpoint genes and susceptibility to HIV-1 infection and AIDS progression from a northern chinese MSM population.AIDS research and therapy · 2023Article
- Bombyx mori Nucleopolyhedrovirus (BmNPV) Induces G2/M Arrest to Promote Viral Multiplication by DepletingInsects · 2021Article
- Article
- Review
- Dual Functionality of HIV-1 Vif in APOBEC3 Counteraction and Cell Cycle Arrest.Frontiers in microbiology · 2020Review
- HIV-1 Vif Triggers Cell Cycle Arrest by Degrading Cellular PPP2R5 Phospho-regulators.Cell reports · 2019Article
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- Mechanisms of HIV-1 Tat neurotoxicity via CDK5 translocation and hyper-activation: role in HIV-associated neurocognitive disorders.Current HIV research · 2015Review
- Overexpression of p42.3 promotes cell growth and tumorigenicity in hepatocellular carcinoma.World journal of gastroenterology · 2013Article
- Toward system-level understanding of baculovirus-host cell interactions: from molecular fundamental studies to large-scale proteomics approaches.Frontiers in microbiology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
The two major cytopathic factors in human immunodeficiency virus type 1 (HIV-1), the accessory proteins viral infectivity factor (Vif) and viral protein R (Vpr), inhibit cell-cycle progression at the G2 phase of the cell cycle. Although Vpr-induced blockade and the associated T-cell death have been well studied, the molecular mechanism of G2 arrest by Vif remains undefined. To elucidate how Vif induces arrest, we infected synchronized Jurkat T-cells and examined the effect of Vif on the activation of Cdk1 and CyclinB1, the chief cell-cycle factors for the G2 to M phase transition. We found that the characteristic dephosphorylation of an inhibitory phosphate on Cdk1 did not occur in infected cells expressing Vif. In addition, the nuclear translocation of Cdk1 and CyclinB1 was disregulated. Finally, Vif-induced cell cycle arrest was correlated with proviral expression of Vif. Taken together, our results suggest that Vif impairs mitotic entry by interfering with Cdk1-CyclinB1 activation.
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Registered trials
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