ArticleJournal of virology2005
Mitogen-activated protein kinases regulate LSF occupancy at the human immunodeficiency virus type 1 promoter.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Ectopic USP15 expression inhibits HIV-1 transcription involving changes in YY1 deubiquitination and stability.Frontiers in cellular and infection microbiology · 2024Article
- Severe acute respiratory syndrome coronavirus 2 may exploit human transcription factors involved in retinoic acid and interferon-mediated response: a hypothesis supported by anNew microbes and new infections · 2021Article
- Article
- Review
- The transcription factor LSF: a novel oncogene for hepatocellular carcinoma.American journal of cancer research · 2012Article
- Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.Molecular biology international · 2012Article
- Mutation of a diacidic motif in SIV-PBj Nef impairs T-cell activation and enteropathic disease.Retrovirology · 2011Article
- Prolyl isomerase Pin1 regulates transcription factor LSF (TFCP2) by facilitating dephosphorylation at two serine-proline motifs.The Journal of biological chemistry · 2010Article
- Transcription factors LSF and E2Fs: tandem cyclists driving G0 to S?Cell cycle (Georgetown, Tex.) · 2009Article
- Binding of LBP-1a to specific immunoglobulin switch regions in vivo correlates with specific repression of class switch recombination.European journal of immunology · 2009Article
- Phosphorylation by cyclin C/cyclin-dependent kinase 2 following mitogenic stimulation of murine fibroblasts inhibits transcriptional activity of LSF during G1 progression.Molecular and cellular biology · 2009Article
- YY1 and FoxD3 regulate antiretroviral zinc finger protein OTK18 promoter activation induced by HIV-1 infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009Article
- Induction of chromosomally integrated HIV-1 LTR requires RBF-2 (USF/TFII-I) and Ras/MAPK signaling.Virus genes · 2007Article
- The regulation of HIV-1 transcription: molecular targets for chemotherapeutic intervention.Medicinal research reviews · 2006Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) establishes a persistent, nonproductive state within a small population of memory CD4(+) cells. The transcription factor LSF binds to sequences within the HIV-1 long terminal repeat (LTR) initiation region and recruits a second factor, YY1, to the LTR. These factors then cooperatively recruit histone deacetylase 1 to the LTR, resulting in inhibition of transcription. This appears to be one mechanism contributing to HIV persistence within resting CD4(+) T cells. We sought to further detail LSF binding to the HIV-1 LTR and factors that regulate LSF occupancy. We find that LSF binds the LTR as a tetramer and that binding is regulated by phosphorylation mediated by mitogen-activated protein kinases (MAPKs). In vitro, phosphorylation of LSF by Erk decreases binding to the LTR, while binding is increased by p38 phosphorylation. LSF occupancy at LTR chromatin is increased by the p38 agonist anisomycin and decreased by specific p38 inhibition. p38 inhibition also results in increased acetylation of histone H4 at the LTR nucleosome adjacent to the LSF binding site. p38 inhibition also blocked the ability of YY1 to inhibit activation of the integrated HIV promoter. Finally, HIV was recovered from the resting CD4(+) T cells of aviremic, HIV-infected donors upon treatment of these cells with specific inhibitor of p38. These data suggest that the MAPK pathway regulates LSF binding to the LTR and thereby one aspect of the regulation of HIV expression. This mechanism could be exploited as a novel therapeutic target to disrupt latent HIV infection.
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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.