ArticleThe EMBO journal1995
HIV-1 Tat potentiates TNF-induced NF-kappa B activation and cytotoxicity by altering the cellular redox state.
Article in The EMBO journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.
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Who cites it
114 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial changes associated with viral infectious diseases in the paediatric population.Reviews in medical virology · 2021Pooled it
- Glutathione deficiency is associated with impaired survival in HIV disease.Proceedings of the National Academy of Sciences of the United States of America · 1997Trial
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- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- Variation in HIV-1 Tat activity is a key determinant in the establishment of latent infection.JCI insight · 2024Article
- ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies.Current issues in molecular biology · 2024Review
- Review
- Unraveling the Role of Reactive Oxygen Species in T Lymphocyte Signaling.International journal of molecular sciences · 2024Review
- Clearance of persistent SARS-CoV-2 associates with increased neutralizing antibodies in advanced HIV disease post-ART initiation.Nature communications · 2024Article
- Tuberculosis and COVID-19 in the elderly: factors driving a higher burden of disease.Frontiers in immunology · 2023Review
- Article
- Citrate shuttling in astrocytes is required for processing cocaine-induced neuron-derived excess peroxidated fatty acids.iScience · 2022Article
- CCR5 antagonist treatment inhibits vascular injury by regulating NADPH oxidase 1.Biochemical pharmacology · 2022Article
- Impact of human immunodeficiency virus on pulmonary vascular disease.Global cardiology science & practice · 2021Review
- Host-virus interaction and viral evasion.Cell biology international · 2021Review
- Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection.International journal of molecular sciences · 2021Review
- Pathogenesis of Human Immunodeficiency Virus-Journal of clinical medicine · 2020Review
- Sex differences and Tat expression affect dopaminergic receptor expression and response to antioxidant treatment in methamphetamine-sensitized HIV Tat transgenic mice.Neuropharmacology · 2020Article
- Article
- The Glutamate System as a Crucial Regulator of CNS Toxicity and Survival of HIV Reservoirs.Frontiers in cellular and infection microbiology · 2020Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study demonstrates that human immunodeficiency virus type 1 (HIV-1) Tat protein amplifies the activity of tumor necrosis factor (TNF), a cytokine that stimulates HIV-1 replication through activation of NF-kappa B. In HeLa cells stably transfected with the HIV-1 tat gene (HeLa-tat cells), expression of the Tat protein enhanced both TNF-induced activation of NF-kappa B and TNF-mediated cytotoxicity. A similar potentiation of TNF effects was observed in Jurkat T cells and HeLa cells treated with soluble Tat protein. TNF-mediated activation of NF-kappa B and cytotoxicity involves the intracellular formation of reactive oxygen intermediates. Therefore, Tat-mediated effects on the cellular redox state were analyzed. In both T cells and HeLa cells HIV-1 Tat suppressed the expression of Mn-dependent superoxide dismutase (Mn-SOD), a mitochondrial enzyme that is part of the cellular defense system against oxidative stress. Thus, Mn-SOD RNA protein levels and activity were markedly reduced in the presence of Tat. Decreased Mn-SOD expression was associated with decreased levels of glutathione and a lower ratio of reduced:oxidized glutathione. A truncated Tat protein (Tat1-72), known to transactivate the HIV-1 long terminal repeat (LTR), no longer affected Mn-SOD expression, the cellular redox state or TNF-mediated cytotoxicity. Thus, our experiments demonstrate that the C-terminal region of HIV-1 Tat is required to suppress Mn-SOD expression and to induce pro-oxidative conditions reflected by a drop in reduced glutathione (GSH) and the GSH:oxidized GSH (GSSG) ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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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.