ArticleJournal of virology2010
Distinct p53, p53:LANA, and LANA complexes in Kaposi's Sarcoma--associated Herpesvirus Lymphomas.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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.
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Who cites it
50 citing papers in PubMed, 72 citations in OpenAlex.
- Comparative study of clinical features, pathology, and immunophenotype between HIV-related cutaneous and visceral Kaposi's sarcoma.BMC cancer · 2026Article
- KSHV and cancer: understanding the oncogenic machinery for next-generation diagnostic tools and therapies.Archives of microbiology · 2026Review
- Recent Advances in Development of Kaposi's Sarcoma-Associated Herpesvirus-Latency-Associated Nuclear Antigen Targeted Therapies.Journal of medical virology · 2025Review
- Molecular Mechanisms of Kaposi Sarcoma-Associated Herpesvirus (HHV8)-Related Lymphomagenesis.Cancers · 2024Review
- The ORF45 Protein of Kaposi's Sarcoma-Associated Herpesvirus and Its Critical Role in the Viral Life Cycle.Viruses · 2022Review
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- The ORF45 Protein of Kaposi Sarcoma-Associated Herpesvirus Is an Inhibitor of p53 Signaling during Viral Reactivation.Journal of virology · 2021Article
- Viral Manipulation of the Host Epigenome as a Driver of Virus-Induced Oncogenesis.Microorganisms · 2021Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Novel modulators of p53-signaling encoded by unknown genes of emerging viruses.PLoS pathogens · 2021Article
- KSHV LANA acetylation-selective acidic domain reader sequence mediates virus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Kaposi's Sarcoma-Associated Herpesvirus LANA Modulates the Stability of the E3 Ubiquitin Ligase RLIM.Journal of virology · 2020Article
- Gene essentiality landscape and druggable oncogenic dependencies in herpesviral primary effusion lymphoma.Nature communications · 2018Article
- Effects of the NEDD8-Activating Enzyme Inhibitor MLN4924 on Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2017Article
- Ribonucleotide reductase represents a novel therapeutic target in primary effusion lymphoma.Oncogene · 2017Article
- Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation.The Journal of antibiotics · 2017Article
- Article
- Regulation of the Abundance of Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein by Oncoprotein MDM2.PLoS pathogens · 2016Article
- KSHV-Mediated Angiogenesis in Tumor Progression.Viruses · 2016Review
- Identification of Kaposi Sarcoma Herpesvirus (KSHV) vIRF1 Protein as a Novel Interaction Partner of Human Deubiquitinase USP7.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The role of p53 in primary effusion lymphoma (PEL) is complicated. The latency-associated nuclear antigen (LANA) of Kaposi's sarcoma-associated herpesvirus (KSHV) binds p53. Despite this interaction, we had found that p53 was functional in PEL, i.e., able to induce apoptosis in response to DNA damage (C. E. Petre, S. H. Sin, and D. P. Dittmer, J. Virol. 81:1912-1922, 2007), and that hdm2 was overexpressed. To further elucidate the relationship between LANA, p53, and hdm2, we purified LANA complexes from PEL by column chromatography. This confirmed that LANA bound p53. However, the LANA:p53 complexes were a minority compared to hdm2:p53 and p53:p53 complexes. The half-life of p53 was not extended, which is in contrast to the half-life of simian virus 40 T antigen-transformed cells. p53:p53, LANA:p53, and LANA:LANA complexes coexisted in PEL, and each protein was able to bind to its cognate DNA element. These data suggest that under normal conditions, p53 is inactive in PEL, thus allowing for exponential growth, but that this inactivation is driven by the relative stoichiometries of LANA, hdm2, and p53. If p53 is activated by DNA damage or nutlin-3a, the complex falls apart easily, and p53 exercises its role as guardian of the genome.
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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.