ArticleJournal of cellular physiology2013
Inhibition of NF-κB activity by HIV-1 Vpr is dependent on Vpr binding protein.
Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- The regulation of cGAS-STING signaling by RNA virus-derived components.Virology journal · 2024Review
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- HIV-1 Vpr-induced DNA damage activates NF-κB through ATM-NEMO independent of cell cycle arrest.bioRxiv : the preprint server for biology · 2024Article
- Enhanced NF-κB activation via HIV-1 Tat-TRAF6 cross-talk.Science advances · 2024Article
- Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIViScience · 2023Article
- SARS-CoV-2, HIV, and HPV: Convergent evolution of selective regulation of cGAS-STING signaling.Journal of medical virology · 2023Review
- Role of Apoptosis in HIV Pathogenesis.Advances in virology · 2022Review
- Diversity in heat shock protein families: functional implications in virus infection with a comprehensive insight of their role in the HIV-1 life cycle.Cell stress & chaperones · 2021Review
- Article
- HCV eradication with IFN-based therapy does not completely restore gene expression in PBMCs from HIV/HCV-coinfected patients.Journal of biomedical science · 2021Article
- Article
- Cross-talk between microglia and neurons regulates HIV latency.PLoS pathogens · 2019Article
- Article
- Primate lentiviruses use at least three alternative strategies to suppress NF-κB-mediated immune activation.PLoS pathogens · 2017Article
- Virion-Associated Vpr Alleviates a Postintegration Block to HIV-1 Infection of Dendritic Cells.Journal of virology · 2017Article
- The Role of HIV Infection in Neurologic Injury.Brain sciences · 2017Review
- Targeting TNF and TNF Receptor Pathway in HIV-1 Infection: from Immune Activation to Viral Reservoirs.Viruses · 2017Review
- Primate Lentiviruses Modulate NF-κB Activity by Multiple Mechanisms to Fine-Tune Viral and Cellular Gene Expression.Frontiers in microbiology · 2017Review
- HIV-1 Vpr Inhibits Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by Inducing MicroRNA miR-942-5p and Activating NF-κB Signaling.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Numerous studies have reported that Vpr alters NF-κB signaling in various cell types, however, the findings have been largely conflicting with reports of both stimulatory and inhibitory effects of Vpr. Our aim was to investigate the role of Vpr signaling in myeloid cells using an adenovirus based expression and indicator system. Our results show that Vpr is inhibitory to NF-κB, however, this effect is dependent on the particular manner of NF-κB stimulation. Consistent with this notion, we report that Vpr has inhibitory effects that are specific to the TNF-α pathway, but not affecting the LPS pathway, suggesting that differential targets of Vpr may exist for NF-κB regulation. Further, we identify VprBP as one possible cellular component of Vpr's regulation of IκBα in response to TNF-α stimulation. We did not identify such a role for HSP27, which instead seems to inhibit Vpr functions. Chronically HIV-1 infected U1 cells with knockdown constructs for Vpr were unexpectedly less responsive to TNF-α mediated viral replication, perhaps suggesting that other HIV-1 components may antagonize these anti-NF-κB effects in infected cells. We hypothesize that Vpr may serve an important role in the context of viral infection and immune function in vivo, through its selective inhibition of NF-κB pathways.
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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.