ArticleNucleic acids research2012
Human immunodeficiency virus-1 Tat activates NF-κB via physical interaction with IκB-α and p65.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 134 citations in OpenAlex.
- Implications of HIV persistence and pathogenesis in microglia.Current opinion in HIV and AIDS · 2026Review
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- Immune Dysregulation in HIV-TB Co-Infection: Role of Cytokines and T Cell Biomarkers-A Narrative Review.Pathogens (Basel, Switzerland) · 2026Review
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
- Structural and Functional Insights into Viral and Fungal Proteins Involved in Chronic Inflammation and Their Biologic Treatments.Pharmaceutics · 2025Review
- CSAD inhibits excessive inflammation during viral infections through the NF-κB signaling pathway.Journal of virology · 2025Article
- The Hallmarks of Ageing in Human Immunodeficiency Virus Infection and the Impact of Antiretroviral Therapy on Telomeres: A Molecular Perspective.Current issues in molecular biology · 2025Review
- FABP5 is a key player in metabolic modulation and NF-κB dependent inflammation driving pleural mesothelioma.Communications biology · 2025Article
- SIV infection induces alterations in gene expression and loss of interneurons in Rhesus Macaque frontal cortex during early systemic infection.Translational psychiatry · 2025Article
- Adenovirus E1B-55K interferes with cellular IκB kinase complex subunit proteins.Frontiers in immunology · 2025Article
- HIV-Tat upregulates the expression of senescence biomarkers in CD4Frontiers in immunology · 2025Article
- Variation in HIV-1 Tat activity is a key determinant in the establishment of latent infection.JCI insight · 2024Article
- Innate Immune Cell Functions Contribute to Spontaneous HIV Control.Current HIV/AIDS reports · 2024Review
- Linear ubiquitination mediates coronavirus NSP14-induced NF-κB activation.Cell communication and signaling : CCS · 2024Article
- Matrix Metalloproteinase-9 Signaling Regulates Colon Barrier Integrity in Models of HIV Infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Nuclear Factor Kappa B p65: A Possible Biomarker for Persistent Inflammation in HIV-1 Infection?Cureus · 2024Review
- Monocyte to macrophage differentiation and changes in cellular redox homeostasis promote cell type-specific HIV latency reactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Enhanced NF-κB activation via HIV-1 Tat-TRAF6 cross-talk.Science advances · 2024Article
- Editorial: Recent advances in diagnosis, prognosis, and therapy of oncogenic virus-driven tumors.Frontiers in oncology · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor (NF)-κB is a master regulator of pro-inflammatory genes and is upregulated in human immunodeficiency virus 1 (HIV-1) infection. Mechanisms underlying the NF-κB deregulation by HIV-1 are relevant for immune dysfunction in AIDS. We report that in single round HIV-1 infection, or single-pulse PMA stimulation, the HIV-1 Tat transactivator activated NF-κB by hijacking the inhibitor IκB-α and by preventing the repressor binding to the NF-κB complex. Moreover, Tat associated with the p65 subunit of NF-κB and increased the p65 DNA-binding affinity and transcriptional activity. The arginine- and cysteine-rich domains of Tat were required for IκB-α and p65 association, respectively, and for sustaining the NF-κB activity. Among an array of NF-κB-responsive genes, Tat mostly activated the MIP-1α expression in a p65-dependent manner, and bound to the MIP-1α NF-κB enhancer thus promoting the recruitment of p65 with displacement of IκB-α; similar findings were obtained for the NF-κB-responsive genes CSF3, LTA, NFKBIA and TLR2. Our results support a novel mechanism of NF-κB activation via physical interaction of Tat with IκB-α and p65, and may contribute to further insights into the deregulation of the inflammatory response by HIV-1.
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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.