ArticleProceedings of the National Academy of Sciences of the United States of America1998
Genes in the pX region of human T cell leukemia virus I influence Vav phosphorylation in T cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- 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
- Human T-lymphotropic virus proteins and post-translational modification pathways.World journal of virology · 2012Review
- Design of versatile biochemical switches that respond to amplitude, duration, and spatial cues.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Role of accessory proteins of HTLV-1 in viral replication, T cell activation, and cellular gene expression.Frontiers in bioscience : a journal and virtual library · 2004Review
- Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity.Retrovirology · 2004Review
- Critical role of human T-lymphotropic virus type 1 accessory proteins in viral replication and pathogenesis.Microbiology and molecular biology reviews : MMBR · 2002Review
- Functional role of pX open reading frame II of human T-lymphotropic virus type 1 in maintenance of viral loads in vivo.Journal of virology · 2000Article
- Induction of adult T-cell leukemia-like lymphoproliferative disease and its inhibition by adoptive immunotherapy in T-cell-deficient nude rats inoculated with syngeneic human T-cell leukemia virus type 1-immortalized cells.Journal of virology · 1999Article
- Mechanisms of T-cell activation by human T-cell lymphotropic virus type I.Microbiology and molecular biology reviews : MMBR · 1999Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T cell leukemia virus I (HTLV-I) causes acute leukemic disease in a low percentage of infected individuals through obscure mechanisms. Our studies compare two rabbit HTLV-I-infected T cell lines: one, RH/K34, causes lethal experimental leukemia and the other, RH/K30, mediates asymptomatic infection. We show herein that the product of the protooncogene vav is constitutively Tyr-phosphorylated in RH/K34 but not in RH/K30. A role for the retrovirus in phosphorylation of Vav was assigned by transfection experiments with molecular clones of HTLV-I derived from the two lines. The HTLV-I molecular clone from RH/K30, but not that from RH/K34, down-regulates Vav phosphorylation in a Herpesvirus ateles-transformed T cell line. Use of recombinant virus clones revealed that a pX region sequence differing by two nucleotides between the two clones mediates this down-regulation. Because Vav is involved in T cell signaling and Vav phosphorylation occurs upon activation of T cells, control of the activation state of Vav by viral proteins may relate to the leukemogenic potential of certain HTLV-I-infected cells.
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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.