ArticleJournal of molecular biology2009
Structural basis of HIV-1 activation by NF-kappaB--a higher-order complex of p50:RelA bound to the HIV-1 LTR.
Article in Journal of molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- HIV-1 Infection Transcriptomics: Meta-Analysis of CD4+ T Cells Gene Expression Profiles.Viruses · 2021Pooled it
- Genistein from Thai Fermented Soybean (Thua-nao) Attenuates Osteoarthritis Pathogenesis via Dual Inhibition of NF-κB and MAPK Signaling: Evidence from Ex Vivo, Computational, and In Vitro Models.Journal of agricultural and food chemistry · 2026Article
- Anti-Inflammatory Effects of Bisacurone Isolated fromMolecules (Basel, Switzerland) · 2026Article
- Oleanolic acid combined with aspirin plays antitumor roles in colorectal cancer via the Akt/NFκB/IκBα/COX2 pathway.Cell death discovery · 2024Article
- Nuclear Factor Kappa B p65: A Possible Biomarker for Persistent Inflammation in HIV-1 Infection?Cureus · 2024Review
- HIV-Infected Hepatic Stellate Cells or HCV-Infected Hepatocytes Are Unable to Promote Latency Reversal among HIV-Infected Mononuclear Cells.Pathogens (Basel, Switzerland) · 2024Article
- ExploringPharmaceuticals (Basel, Switzerland) · 2024Article
- Development trends of immune activation during HIV infection in recent three decades: a bibliometric analysis based on CiteSpace.Archives of microbiology · 2023Article
- Enhanced Transcriptional Strength of HIV-1 Subtype C Minimizes Gene Expression Noise and Confers Stability to the Viral Latent State.Journal of virology · 2023Article
- Computational evaluation of bioactive compounds inBiotechnologia · 2023Article
- Article
- Repression of HIV-1 reactivation mediated by CRISPR/dCas9-KRAB in lymphoid and myeloid cell models.Retrovirology · 2022Article
- Irreversible Loss of HIV-1 Proviral Competence in Myeloid Cells upon Suppression of NF-κB Activity.Journal of virology · 2022Article
- Possible Interaction of Nonsteroidal Anti-inflammatory Drugs Against NF-κB- and COX-2-Mediated Inflammation: In Silico Probe.Applied biochemistry and biotechnology · 2022Article
- xCT/SLC7A11 antiporter function inhibits HIV-1 infection.Virology · 2021Article
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Extracellular Vesicles as a New Promising Therapy in HIV Infection.Frontiers in immunology · 2021Review
- Bidirectional Associations among Nicotine and Tobacco Smoke, NeuroHIV, and Antiretroviral Therapy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- First Responders Shape a Prompt and Sharp NF-κB-Mediated Transcriptional Response to TNF-α.iScience · 2020Article
- A Stronger Transcription Regulatory Circuit of HIV-1C Drives the Rapid Establishment of Latency with Implications for the Direct Involvement of Tat.Journal of virology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The activation and latency of human immunodeficiency virus type 1 (HIV-1) are tightly controlled by the transcriptional activity of its long terminal repeat (LTR) region. The LTR is regulated by viral proteins as well as host factors, including the nuclear factor kappaB (NF-kappaB) that becomes activated in virus-infected cells. The two tandem NF-kappaB sites of the LTR are among the most highly conserved sequence elements of the HIV-1 genome. Puzzlingly, these sites are arranged in a manner that seems to preclude simultaneous binding of both sites by NF-kappaB, although previous biochemical work suggests otherwise. Here, we have determined the crystal structure of p50:RelA bound to the tandem kappaB element of the HIV-1 LTR as a dimeric dimer, providing direct structural evidence that NF-kappaB can occupy both sites simultaneously. The two p50:RelA dimers bind the adjacent kappaB sites and interact through a protein contact that is accommodated by DNA bending. The two dimers clamp DNA from opposite faces of the double helix and form a topological trap of the bound DNA. Consistent with these structural features, our biochemical analyses indicate that p50:RelA binds the HIV-1 LTR tandem kappaB sites with an apparent anti-cooperativity but enhanced kinetic stability. The slow on and off rates we observe may be relevant to viral latency because viral activation requires sustained NF-kappaB activation. Furthermore, our work demonstrates that the specific arrangement of the two kappaB sites on the HIV-1 LTR can modulate the assembly kinetics of the higher-order NF-kappaB complex on the viral promoter. This phenomenon is unlikely restricted to the HIV-1 LTR but probably represents a general mechanism for the function of composite DNA elements in transcription.
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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.