ArticleCell cycle (Georgetown, Tex.)2010
Activation of HIV-1 LTR by Rad51 in microglial cells.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- BRCA1-RAD51 homologous DNA repair pathway promotes HIV-1 reverse transcription.Science advances · 2026Article
- Bloom syndrome helicase is required for efficient HIV-1 reverse transcription in macrophages.bioRxiv : the preprint server for biology · 2026Article
- Review
- The DNA damage response promotes polyomavirus JC infection by nucleus to cytoplasm NF- kappaB activation.Virology journal · 2017Article
- A novel role for the DNA repair gene Rad51 in Netrin-1 signalling.Scientific reports · 2017Article
- Dual and Opposite Effects of hRAD51 Chemical Modulation on HIV-1 Integration.Chemistry & biology · 2015Article
- The dual action of poly(ADP-ribose) polymerase -1 (PARP-1) inhibition in HIV-1 infection: HIV-1 LTR inhibition and diminution in Rho GTPase activity.Frontiers in microbiology · 2015Article
- Cancer risk at low doses of ionizing radiation: artificial neural networks inference from atomic bomb survivors.Journal of radiation research · 2014Review
- Rad51 activates polyomavirus JC early transcription.PloS one · 2014Article
- Article
- Stimulation of the human RAD51 nucleofilament restricts HIV-1 integration in vitro and in infected cells.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection with HIV-1 induces a variety of biological alterations to the host that are beneficial to the life cycle of the virus but may have adverse effects on the host cell. Here we demonstrate that expression of Rad51, a major component of the homologous recombination-directed DNA repair (HRR) pathway, is induced upon HIV-1 infection of microglial cells. Activation of Rad51 expression positively impacts on HIV-1 LTR transcription through a region of the viral promoter known for binding the inducible transcription factor NFκB. Rad51 showed the ability to form a complex with the p65 subunit of NFκB and regulate the level of p65 interaction with LTR DNA encompassing the κB motif. This study provides evidence for reciprocal interaction of HIV-1 and a host DNA repair protein that impacts on expression of the viral genome. These results also point to the ability of HIV-1 to recruit proteins involved in DNA repair that are necessary for retroviral DNA integration, efficient replication and prevention of viral-induced cell death.
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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.