ArticleThe Journal of biological chemistry2010
Combinatorial signals from CD28 differentially regulate human immunodeficiency virus transcription in T cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Study of the Genetic Expression of Antiretroviral Restriction Factors and Acute Phase Proteins in Cattle Infected with Bovine Leukemia Virus.Pathogens (Basel, Switzerland) · 2023Article
- New insights into transcription elongation control of HIV-1 latency and rebound.Trends in immunology · 2023Review
- CD4AIDS research and human retroviruses · 2018Review
- Mechanism and factors that control HIV-1 transcription and latency activation.Journal of Zhejiang University. Science. B · 2014Review
- Transcriptional control of HIV latency: cellular signaling pathways, epigenetics, happenstance and the hope for a cure.Virology · 2014Review
- Viral-host interactions that control HIV-1 transcriptional elongation.Chemical reviews · 2013Review
- Negative elongation factor (NELF) coordinates RNA polymerase II pausing, premature termination, and chromatin remodeling to regulate HIV transcription.The Journal of biological chemistry · 2013Article
- Control of HIV latency by epigenetic and non-epigenetic mechanisms.Current HIV research · 2011Article
- T-cell receptor signaling enhances transcriptional elongation from latent HIV proviruses by activating P-TEFb through an ERK-dependent pathway.Journal of molecular biology · 2011Article
- New insights into the control of HIV-1 transcription: when Tat meets the 7SK snRNP and super elongation complex (SEC).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- Inequalities and duality in gene coexpression networks of HIV-1 infection revealed by the combination of the double-connectivity approach and the Gini's method.Journal of biomedicine & biotechnology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation through the T-cell receptor and the costimulatory receptor CD28 supports efficient HIV transcription as well as reactivation of latent provirus. To characterize critical signals associated with CD28 that regulate HIV-1 transcription, we generated a library of chimeric CD28 receptors that harbored different combinations of key tyrosine residues in the cytoplasmic tail, Tyr-173, Tyr-188, Tyr-191, and Tyr-200. We found that Tyr-191 and Tyr-200 induce HIV-1 transcription via the activation of NF-kappaB and its recruitment to the HIV-long terminal repeat. Tyr-188 modifies positive and negative signals associated with CD28. Importantly, signaling through Tyr-188, Tyr-191, and Tyr-200 is required to overcome the inhibition posed by Tyr-173. CD28 also regulates P-TEFb activity, which is necessary for HIV-1 transcription processivity, by limiting the release of P-TEFb from the HEXIM1-7SK inhibitory complex in response to T-cell receptor signaling. Our studies reveal that CD28 regulates HIV-1 provirus transcription through a complex interplay of positive and negative signals that may be manipulated to control HIV-1 transcription and replication.
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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.