ArticlePloS one2011
Opposite effects of HIV-1 p17 variants on PTEN activation and cell growth in B cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Role of HIV-1 matrix protein p17 variants in lymphoma pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2015Trial
- Decoding HIV-1 Next Move Through Matrix Protein p17 Quasi-Species.MicrobiologyOpen · 2026Article
- Beyond Viral Assembly: The Emerging Role of HIV-1 p17 in Vascular Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- Circulating Biomarker Panorama in HIV-Associated Lymphoma: A Bridge from Early Risk Warning to Prognostic Stratification.Biomolecules · 2025Review
- Lymphoproliferations in People Living with HIV: Oncogenic Pathways, Diagnostic Challenges, and New Therapeutic Opportunities.Cancers · 2025Review
- Pathological Mechanisms Involved in HIV-Associated Lymphomagenesis: Novel Targeted Therapeutic Approaches.Cells · 2025Review
- Review
- Virus-driven dysregulation of the BCR pathway: a potential mechanism for the high prevalence of HIV related B-cell lymphoma.Annals of hematology · 2024Review
- Molecular Mechanisms Involved in the B Cell Growth and Clonogenic Activity of HIV-1 Matrix Protein p17 Variants.Viruses · 2024Article
- HIV-1 Structural Proteins or Cell-Signaling Factors? That Is the Question!Current issues in molecular biology · 2024Review
- Article
- HIV-1 mutants expressing B cell clonogenic matrix protein p17 variants are increasing their prevalence worldwide.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- B-cell clonogenic activity of HIV-1 p17 variants is driven by PAR1-mediated EGF transactivation.Cancer gene therapy · 2021Article
- Heparin and heparan sulfate proteoglycans promote HIV-1 p17 matrix protein oligomerization: computational, biochemical and biological implications.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
- A single amino acid substitution confers B-cell clonogenic activity to the HIV-1 matrix protein p17.Scientific reports · 2017Article
- Lung cancer in persons with HIV.Current opinion in HIV and AIDS · 2017Review
- HIV-1 matrix protein p17 and its variants promote human triple negative breast cancer cell aggressiveness.Infectious agents and cancer · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HIV-1 matrix protein p17 is a structural protein that can act in the extracellular environment to deregulate several functions of immune cells, through the interaction of its NH(2)-terminal region with a cellular surface receptor (p17R). The intracellular events triggered by p17/p17R interaction have been not completely characterized yet. In this study we analyze the signal transduction pathways induced by p17/p17R interaction and show that in Raji cells, a human B cell line stably expressing p17R on its surface, p17 induces a transient activation of the transcriptional factor AP-1. Moreover, it was found to upregulate pERK1/2 and downregulate pAkt, which are the major intracellular signalling components involved in AP-1 activation. These effects are mediated by the COOH-terminal region of p17, which displays the capability of keeping PTEN, a phosphatase that regulates the PI3K/Akt pathway, in an active state through the serine/threonine (Ser/Thr) kinase ROCK. Indeed, the COOH-terminal truncated form of p17 (p17Δ36) induced activation of the PI3K/Akt pathway by maintaining PTEN in an inactive phosphorylated form. Interestingly, we show that among different p17s, a variant derived from a Ugandan HIV-1 strain, named S75X, triggers an activation of PI3K/Akt signalling pathway, and leads to an increased B cell proliferation and malignant transformation. In summary, this study shows the role of the COOH-terminal region in modulating the p17 signalling pathways so highlighting the complexity of p17 binding to and signalling through its receptor(s). Moreover, it provides the first evidence on the presence of a p17 natural variant mimicking the p17Δ36-induced signalling in B cells and displaying the capacity of promoting B cell growth and tumorigenesis.
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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.