ArticleVirology journal2008
Drug 9AA reactivates p21/Waf1 and Inhibits HIV-1 progeny formation.
Article in Virology journal, 2008. 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, 19 citations in OpenAlex.
- HIV-1-related factors interact with p53 to influence cellular processes.AIDS research and therapy · 2023Review
- Review
- Select host restriction factors are associated with HIV persistence during antiretroviral therapy.AIDS (London, England) · 2015Article
- Eradication of HIV and Cure of AIDS, Now and How?Frontiers in immunology · 2013Review
- Role of cellular iron and oxygen in the regulation of HIV-1 infection.Future virology · 2013Article
- Article
- Article
- 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
- 9-Aminoacridine inhibition of HIV-1 Tat dependent transcription.Virology journal · 2009Article
- Small-molecule inhibitor which reactivates p53 in human T-cell leukemia virus type 1-transformed cells.Journal of virology · 2008Article
- Chromatin dynamics associated with HIV-1 Tat-activated transcription.Biochimica et biophysica actaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been demonstrated that the p53 pathway plays an important role in HIV-1 infection. Previous work from our lab has established a model demonstrating how p53 could become inactivated in HIV-1 infected cells through binding to Tat. Subsequently, p53 was inactivated and lost its ability to transactivate its downstream target gene p21/waf1. P21/waf1 is a well-known cdk inhibitor (CKI) that can lead to cell cycle arrest upon DNA damage. Most recently, the p21/waf1 function was further investigated as a molecular barrier for HIV-1 infection of stem cells. Therefore, we reason that the restoration of the p53 and p21/waf1 pathways could be a possible theraputical arsenal for combating HIV-1 infection. In this current study, we show that a small chemical molecule, 9-aminoacridine (9AA) at low concentrations, could efficiently reactivate p53 pathway and thereby restoring the p21/waf1 function. Further, we show that the 9AA could significantly inhibit virus replication in activated PBMCs, likely through a mechanism of inhibiting the viral replication machinery. A mechanism study reveals that the phosphorylated p53ser15 may be dissociated from binding to HIV-1 Tat protein, thereby activating the p21/waf1 gene. Finally, we also show that the 9AA-activated p21/waf1 is recruited to HIV-1 preintegration complex, through a mechanism yet to be elucidated.
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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.