ArticleBlood2013
PA28γ is a novel corepressor of HTLV-1 replication and controls viral latency.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
15 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- HTLV-1 Tax Tug-of-War: Cellular Senescence and Death or Cellular Transformation.Pathogens (Basel, Switzerland) · 2024Review
- New Safety Aspects in Corneal Donation-Studies on SARS-CoV-2-Positive Corneal Donors.Journal of clinical medicine · 2022Article
- Transcription Independent Stimulation of Telomerase Enzymatic Activity by HTLV-I Tax Through Stimulation of IKK.Journal of cancer sciences · 2021Article
- Race to arsenal COVID-19 therapeutics: Current alarming status and future directions.Chemico-biological interactions · 2020Review
- Proteasome activator PA28γ-dependent degradation of coronavirus disease (COVID-19) nucleocapsid protein.Biochemical and biophysical research communications · 2020Article
- PA28γ, an Accomplice to Malignant Cancer.Frontiers in oncology · 2020Review
- NOTCH1 Activation Depletes the Pool of Side Population Stem Cells in ATL.Journal of cancer sciences · 2017Article
- Multiple Pathways Control the Reactivation of Telomerase in HTLV-I-Associated Leukemia.International journal of cancer and oncology · 2015Article
- STAT1: A Novel Target of miR-150 and miR-223 Is Involved in the Proliferation of HTLV-I-Transformed and ATL Cells.Neoplasia (New York, N.Y.) · 2015Article
- miR-28-3p is a cellular restriction factor that inhibits human T cell leukemia virus, type 1 (HTLV-1) replication and virus infection.The Journal of biological chemistry · 2015Article
- Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.Journal of oncology · 2015Review
- Increased proteasome activator 28 gamma (PA28γ) levels are unspecific but correlate with disease activity in rheumatoid arthritis.BMC musculoskeletal disorders · 2014Article
- Tax impairs DNA replication forks and increases DNA breaks in specific oncogenic genome regions.Molecular cancer · 2014Article
- The need to accessorize: molecular roles of HTLV-1 p30 and HTLV-2 p28 accessory proteins in the viral life cycle.Frontiers in microbiology · 2013Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledThe establishment of a latent reservoir by human tumor viruses is a vital step in initiating cellular transformation and represents a major shortcoming to current therapeutic strategies and the ability to eradicate virus-infected cells. Human T-cell leukemia virus type 1 (HTLV-1) establishes a lifelong infection and is linked to adult T-cell leukemia lymphoma (ATLL). Here, we demonstrate that HTLV-1 p30 recruits the cellular proteasome activator PA28γ onto the viral tax/rex mRNA to prevent its nuclear export and suppress virus replication. Interaction of p30 with a PA28γ retaining fully functional proteasome activity is required for p30's ability to repress HTLV-1. Consistently, HTLV-1 molecular clones replicate better and produce more virus particles in PA28γ-deficient cells. These results define a unique and novel role for the cellular factor PA28γ in the control of nuclear RNA trafficking and HTLV-1–induced latency. Importantly, knockdown of PA28γ expression in ATLL cells latently infected with HTLV-1 reactivates expression of viral tax/rex RNA and the Tax protein. Because Tax is the most immunogenic viral antigen and triggers strong CTL responses, our results suggest that PA28γ-targeted therapy may reactivate virus expression from latently infected cells and allow their eradication from the host. KEY POINTS: PA28γ acts as a co-repressor of HTLV-1 p30 to suppress virus replication and is required for the maintenance of viral latency. HTLV-1 has evolved a unique function mediated by its posttranscriptional repressor p30, which is not found in HTLV-2.
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Registered trials
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.