ArticleJournal of virology2021
Tax Induces the Recruitment of NF-κB to Unintegrated HIV-1 DNA To Rescue Viral Gene Expression and Replication.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 13 citations in OpenAlex.
- Non-integrase mechanisms for dolutegravir resistance.Retrovirology · 2026Review
- PTEN Mediates the Silencing of Unintegrated HIV-1 DNA.Viruses · 2024Article
- HIV-1 3'-Polypurine Tract Mutations Confer Dolutegravir Resistance by Switching to an Integration-Independent Replication Mechanism via 1-LTR Circles.Journal of virology · 2023Article
- HIV Preintegration Transcription and Host Antagonism.Current HIV research · 2023Article
- Mutations in the 3'-PPT Lead to HIV-1 Replication without Integration.Journal of virology · 2022Article
- Two lymphoid cell lines potently silence unintegrated HIV-1 DNAs.Retrovirology · 2022Article
- Multimodal Functionalities of HIV-1 Integrase.Viruses · 2022Review
- Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin.Journal of molecular biology · 2022Review
- CHAF1A/B mediate silencing of unintegrated HIV-1 DNAs early in infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mutations in the HIV-1 3'-Polypurine Tract Can Confer Dolutegravir Resistance.Antimicrobial agents and chemotherapy · 2022Article
- Epigenetic Regulation of Human T-Cell Leukemia Virus Gene Expression.Microorganisms · 2021Review
- Silencing of Unintegrated Retroviral DNAs.Viruses · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that the normally essential step of integration of the HIV-1 proviral DNA intermediate into the host cell genome becomes dispensable in T cells that express the human T cell leukemia virus 1 (HTLV-1) Tax protein, a known activator of cellular NF-κB. The rescue of integrase (IN)-deficient HIV-1 replication by Tax results from the strong activation of transcription from the long terminal repeat (LTR) promoter on episomal HIV-1 DNA, an effect that is closely correlated with the recruitment of activating epigenetic marks, such as H3Ac, and depletion of repressive epigenetic marks, such as H3K9me3, from chromatinized unintegrated proviruses. In addition, activation of transcription from unintegrated HIV-1 DNA coincides with the recruitment of NF-κB to the two NF-κB binding sites found in the HIV-1 LTR enhancer. Here, we report that the recruitment of NF-κB to unintegrated viral DNA precedes, and is a prerequisite for, Tax-induced changes in epigenetic marks, so that an IN
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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.