ArticleJournal of immunology (Baltimore, Md. : 1950)2008
HIV-1 Tat mediates degradation of RON receptor tyrosine kinase, a regulator of inflammation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- The balance between gasdermin D and STING signaling shapes the severity of schistosome immunopathology.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Prevalence and Associated Factors of Metabolic Syndrome among Patients with Severe Mental Illness Attending a Tertiary Hospital in Southwest Uganda.BioMed research international · 2019Article
- Proteasomal Degradation Machinery: Favorite Target of HIV-1 Proteins.Frontiers in microbiology · 2018Review
- HIV‑1 downregulates the expression and phosphorylation of receptor tyrosine kinase by targeting the NF‑κB pathway.Molecular medicine reports · 2016Article
- Interaction between Tat and Drugs of Abuse during HIV-1 Infection and Central Nervous System Disease.Frontiers in microbiology · 2015Review
- Metabolic syndrome in HIV-infected individuals: underlying mechanisms and epidemiological aspects.AIDS research and therapy · 2013Article
- RON receptor tyrosine kinase, a negative regulator of inflammation, is decreased during simian immunodeficiency virus-associated central nervous system disease.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Immune regulation and evasion of Mammalian host cell immunity during viral infection.Indian journal of virology : an official organ of Indian Virological Society · 2013Article
- Proteasome inhibition in vivo promotes survival in a lethal murine model of severe acute respiratory syndrome.Journal of virology · 2010Article
- Homeostatic chemokines CCL19 and CCL21 promote inflammation in human immunodeficiency virus-infected patients with ongoing viral replication.Clinical and experimental immunology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
HIV encodes several proteins, including Tat, that have been demonstrated to modulate the expression of receptors critical for innate immunity, including MHC class I, mannose receptor, and beta(2)-microglobulin. We demonstrate that Tat targets the receptor tyrosine kinase recepteur d'origine nantais (RON), which negatively regulates inflammation and HIV transcription, for proteosome degradation. Tat decreases cell surface RON expression in HIV-infected monocytic cells, and Tat-mediated degradation of RON protein is blocked by inhibitors of proteosome activity. Tat specifically induced down-regulation of RON and not other cell surface receptors, such as the transferrin receptor, the receptor tyrosine kinase TrkA, or monocytic markers CD14 and ICAM-1. The Tat trans activation domain is required for RON degradation, and this down-regulation is dependent on the integrity of the kinase domain of RON receptor. We propose that Tat mediates degradation of RON through a ubiquitin-proteosome pathway, and suggest that by targeting signals that modulate inflammation, Tat creates a microenvironment that is optimal for HIV replication and progression of AIDS-associated diseases.
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Registered trials
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