ArticleJournal of virology2007
Inhibition of T-cell receptor signal transduction and viral expression by the linker for activation of T cells-interacting p12(I) protein of human T-cell leukemia/lymphoma virus type 1.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 58 citations in OpenAlex.
- HTLV-1 p12 is cleaved to p8 by the signal peptidase complex and its inhibition impairs p8-dependent transmission.PLoS pathogens · 2025Article
- High expression of Rex-orf-I and HBZ mRNAs and bronchiectasis in lung of HTLV-1A/C infected macaques.Nature communications · 2025Article
- Article
- Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024Article
- Vav proteins do not influence dengue virus replication but are associated with induction of phospho-ERK, IL-6, and viperin mRNA following DENV infectionMicrobiology spectrum · 2024Article
- HTLV-1 p12 modulates the levels of prion protein (PrPFrontiers in microbiology · 2023Article
- Hijacking Host Immunity by the Human T-Cell Leukemia Virus Type-1: Implications for Therapeutic and Preventive Vaccines.Viruses · 2022Review
- NK cells and monocytes modulate primary HTLV-1 infection.PLoS pathogens · 2022Article
- Transient Viral Activation in Human T Cell Leukemia Virus Type 1-Infected Macaques Treated With Pomalidomide.Frontiers in medicine · 2022Article
- Transfer of HTLV-1 p8 and Gag to target T-cells depends on VASP, a novel interaction partner of p8.PLoS pathogens · 2020Article
- Role of HTLV-1 orf-I encoded proteins in viral transmission and persistence.Retrovirology · 2019Review
- Non-Structural Proteins from Human T-cell Leukemia Virus Type 1 in Cellular Membranes-Mechanisms for Viral Survivability and Proliferation.International journal of molecular sciences · 2018Review
- Masters of manipulation: Viral modulation of the immunological synapse.Cellular microbiology · 2018Review
- Inhibition of Tunneling Nanotube (TNT) Formation and Human T-cell Leukemia Virus Type 1 (HTLV-1) Transmission by Cytarabine.Scientific reports · 2018Article
- Quantitating the Transfer of the HTLV-1 p8 Protein Between T-Cells by Flow Cytometry.Frontiers in microbiology · 2018Article
- Assessment of HTLV-1 proviral load, LAT, BIM, c-FOS and RAD51 gene expression in adult T cell leukemia/lymphoma.Medical microbiology and immunology · 2017Article
- Review
- Discovery and characterization of auxiliary proteins encoded by type 3 simian T-cell lymphotropic viruses.Journal of virology · 2015Article
- Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In Vivo Model.PloS one · 2015Article
- Co-dependence of HTLV-1 p12 and p8 functions in virus persistence.PLoS pathogens · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The p12(I) protein of human T-cell leukemia/lymphoma virus type 1 (HTLV-1) is a small oncoprotein that increases calcium release following protein kinase C activation by phorbol myristate acetate, and importantly, this effect is linker for activation of T cells (LAT) independent. Here, we demonstrate that p12(I) inhibits the phosphorylation of LAT, Vav, and phospholipase C-gamma 1 and decreases NFAT (nuclear factor of activated T cells) activation upon engagement of the T-cell receptor (TCR) with anti-CD3 antibody. Furthermore, we demonstrate that p12(I) localizes to membrane lipid rafts and, upon engagement of the TCR, relocalizes to the interface between T cells and antigen-presenting cells, defined as the immunological synapse. A p12(I) knockout molecular clone of HTLV-1 expresses more virus upon antigen stimulation than the isogenic wild type, suggesting that, by decreasing T-cell responsiveness, p12(I) curtails viral expression. Thus, p12(I) has contrasting effects on TCR signaling: it down-regulates TCR in a LAT-dependent manner on one hand, and on the other, it increases calcium release in a LAT-independent manner. The negative regulation of T-cell activation by p12(I) may have evolved to minimize immune recognition of infected CD4(+) T cells, to impair the function of infected cytotoxic CD8(+) T cells, and to favor viral persistence in the infected host.
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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.