ArticleJournal of virology2000
Loss of G(1)/S checkpoint in human immunodeficiency virus type 1-infected cells is associated with a lack of cyclin-dependent kinase inhibitor p21/Waf1.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- The Immunogenic Role of Self-DNA in T Cell Immunity.Clinical reviews in allergy & immunology · 2025Review
- Cyclin Dependent Kinases in Antiviral Drug Discovery.Current medicinal chemistry · 2025Review
- Review
- Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin.Journal of molecular biology · 2022Review
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- HIV-1 Tat Recruits HDM2 E3 Ligase To Target IRF-1 for Ubiquitination and Proteasomal Degradation.mBio · 2016Article
- Improvements and Limitations of Humanized Mouse Models for HIV Research: NIH/NIAID "Meet the Experts" 2015 Workshop Summary.AIDS research and human retroviruses · 2016Article
- Potential of Radiation-Induced Cellular Stress for Reactivation of Latent HIV-1 and Killing of Infected Cells.AIDS research and human retroviruses · 2016Article
- Therapeutic doses of irradiation activate viral transcription and induce apoptosis in HIV-1 infected cells.Virology · 2015Article
- Role of Bruton's tyrosine kinase inhibitors in HIV-1-infected cells.Journal of neurovirology · 2015Article
- Hematopoietic Stem and Immune Cells in Chronic HIV Infection.Stem cells international · 2015Review
- Article
- CHK2 kinase in the DNA damage response and beyond.Journal of molecular cell biology · 2014Review
- HIV-associated neuropathogenesis: a systems biology perspective for modeling and therapy.Bio Systems · 2014Review
- Roles and functions of HIV-1 Tat protein in the CNS: an overview.Virology journal · 2013Review
- Host hindrance to HIV-1 replication in monocytes and macrophages.Retrovirology · 2010Review
- Inhibition of human immunodeficiency virus type-1 by cdk inhibitors.AIDS research and therapy · 2010Article
- The CDK inhibitor p21Cip1/WAF1 is induced by FcgammaR activation and restricts the replication of human immunodeficiency virus type 1 and related primate lentiviruses in human macrophages.Journal of virology · 2009Article
- Novel HIV-1 therapeutics through targeting altered host cell pathways.Expert opinion on biological therapy · 2009Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
Productive high-titer infection by human immunodeficiency virus type 1 (HIV-1) requires the activation of target cells. Infection of quiescent peripheral CD4 lymphocytes by HIV-1 results in incomplete, labile reverse transcripts and lack of viral progeny formation. An interplay between Tat and p53 has previously been reported, where Tat inhibited the transcription of the p53 gene, which may aid in the development of AIDS-related malignancies, and p53 expression inhibited HIV-1 long terminal repeat transcription. Here, by using a well-defined and -characterized stress signal, gamma irradiation, we find that upon gamma irradiation, HIV-1-infected cells lose their G(1)/S checkpoints, enter the S phase inappropriately, and eventually apoptose. The loss of the G(1)/S checkpoint is associated with a loss of p21/Waf1 protein and increased activity of a major G(1)/S kinase, namely, cyclin E/cdk2. The p21/Waf1 protein, a known cyclin-dependent kinase inhibitor, interacts with the cdk2/cyclin E complex and inhibits progression of cells into S phase. We find that loss of the G(1)/S checkpoint in HIV-1-infected cells may in part be due to Tat's ability to bind p53 (a known activator of the p21/Waf1 promoter) and sequester its transactivation activity, as seen in both in vivo and in vitro transcription assays. The loss of p21/Waf1 in HIV-1-infected cells was specific to p21/Waf1 and did not occur with other KIP family members, such as p27 (KIP1) and p57 (KIP2). Finally, the advantage of a loss of the G(1)/S checkpoint for HIV-1 per se may be that it pushes the host cell into the S phase, which may then allow subsequent virus-associated processes, such as RNA splicing, transport, translation, and packaging of virion-specific genes, to occur.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.