ArticleCellular microbiology2008
HIV-1 matrix protein p17 binds to monocytes and selectively stimulates MCP-1 secretion: role of transcriptional factor AP-1.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Beyond Viral Assembly: The Emerging Role of HIV-1 p17 in Vascular Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- HIV-1 Structural Proteins or Cell-Signaling Factors? That Is the Question!Current issues in molecular biology · 2024Review
- The cytokine/chemokine response inHeliyon · 2023Review
- Consequences of HIV infection in the bone marrow niche.Frontiers in immunology · 2023Review
- Article
- The HIV-1 Matrix Protein p17 Does Cross the Blood-Brain Barrier.Journal of virology · 2022Article
- Evolution toward beta common chain receptor usage links the matrix proteins of HIV-1 and its ancestors to human erythropoietin.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Role of Autophagy in Von Willebrand Factor Secretion by Endothelial Cells and in the In Vivo Thrombin-Antithrombin Complex Formation Promoted by the HIV-1 Matrix Protein p17.International journal of molecular sciences · 2020Article
- The interleukin-33-mediated inhibition of expression of two key genes implicated in atherosclerosis in human macrophages requires MAP kinase, phosphoinositide 3-kinase and nuclear factor-κB signaling pathways.Scientific reports · 2019Article
- p17 from HIV induces brain endothelial cell angiogenesis through EGFR-1-mediated cell signalling activation.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- HIV-1 matrix protein p17 misfolding forms toxic amyloidogenic assemblies that induce neurocognitive disorders.Scientific reports · 2017Article
- HIV-1 matrix protein p17 and its variants promote human triple negative breast cancer cell aggressiveness.Infectious agents and cancer · 2017Article
- Cellular aspartyl proteases promote the unconventional secretion of biologically active HIV-1 matrix protein p17.Scientific reports · 2016Article
- Endogenous CCL2 neutralization restricts HIV-1 replication in primary human macrophages by inhibiting viral DNA accumulation.Retrovirology · 2015Article
- Simian immunodeficiency virus and human immunodeficiency virus type 1 matrix proteins specify different capabilities to modulate B cell growth.Journal of virology · 2014Article
- Monocytes as regulators of inflammation and HIV-related comorbidities during cART.Journal of immunology research · 2014Review
- HIV-1 matrix protein p17 promotes angiogenesis via chemokine receptors CXCR1 and CXCR2.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Deployment of the human immunodeficiency virus type 1 protein arsenal: combating the host to enhance viral transcription and providing targets for therapeutic development.The Journal of general virology · 2012Article
- The HIV matrix protein p17 subverts nuclear receptors expression and induces a STAT1-dependent proinflammatory phenotype in monocytes.PloS one · 2012Article
- Opposite effects of HIV-1 p17 variants on PTEN activation and cell growth in B cells.PloS one · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 matrix protein p17 activates a variety of cell responses which play a critical role in viral replication and infection. Its activity depends on the expression of p17 receptors (p17R) on the surface of target cells. Whether p17 also plays a role in stimulating human monocytes, a major HIV-1 reservoir, is not known. Here we show that human monocytes constitutively express p17Rs and that p17 selectively triggers these cells to produce MCP-1. The effect of p17 on MCP-1 expression was observed at the transcriptional level and was primarily dependent on the activation of the transcription factor AP-1. p17 increased the binding activity of AP-1 complexes in a time- and dose-dependent manner. Deletion of the AP-1 binding sites in the MCP-1 promoter resulted in the lack of p17-induced MCP-1 transcription. In particular, the P3 binding site located between -69 and -63 position seems to be essential to MCP-1 mRNA induction in p17-treated monocytes. An ever increasing amount of evidences shows a tight link between biologically dysregulated monocytes, AP-1 activation, MCP-1 release and HIV-1 pathogenesis. Overall our results suggest that p17 may play a critical role in the monocyte-mediated inflammatory processes, which are suspected to be major precipitating events in AIDS-defining diseases.
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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.