Evidence map›Paper›PMID 23152516›Full record

ArticleJournal of virology2013

Acetylation of conserved lysines in bovine papillomavirus E2 by p300.

Edward J Quinlan, Sara P Culleton, Shwu-Yuan Wu, Cheng-Ming Chiang, Elliot J Androphy

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. Review
  5. The Role of Tricarboxylic Acid Cycle Metabolites in Viral Infections.Frontiers in cellular and infection microbiology · 2021
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 1 country.

Edward J QuinlanDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Sara P Culleton
Shwu-Yuan Wu
Cheng-Ming Chiang
Elliot J Androphy
Harold C. Simmons Comprehensive Cancer CenterIndiana University – Purdue University Indianapolis · USIndiana University School of MedicineUniversity of Massachusetts Chan Medical School · US

Funding

Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
CONTROL OF PAPILLOMAVIRUS EXPRESSION AND TRANSFORMATIONR01CA058376 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ANDROPHY, ELLIOT J. · 1993 to 2019
$5.7M
E2-Cellular Complexes in HPV Chromatin TranscriptionR01CA103867 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHIANG, CHENG-MING · 2004 to 2017
$4.0M
Regulation of p53 Transcription by Viral Oncoproteins & Covalent ModificationsR01CA124760 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI CHIANG, CHENG-MING · 2007 to 2012
$1.6M
NCI NIH HHS R01 CA058376NCI NIH HHS R01 CA103867NCI NIH HHS R01CA103867NCI NIH HHS R01 CA124760NCI NIH HHS R01CA124760NCI NIH HHS R01CA58376NIAID NIH HHS T32 AI 060519NIAID NIH HHS T32 AI060519
6 · The paper itself

Abstract

The p300, CBP, and pCAF lysine acetyltransferase (KAT) proteins have been reported to physically interact with bovine (BPV) and human (HPV) papillomavirus E2 proteins. While overexpression of these KAT proteins enhances E2-dependent transcription, the mechanism has not been determined. Using RNA interference (RNAi) to deplete these factors, we demonstrated that E2 transcriptional activity requires physiological levels of p300, CBP, and pCAF. Each protein appears to have a unique function in E2-dependent transcription, since overexpression of one KAT failed to compensate for RNAi knockdown of another KAT. Using an in vitro acetylation assay, we identified highly conserved lysines that are targeted by p300 for acetylation. The conservative changes of lysines at positions 111 and 112 to arginine were of particular interest. The K111R and the K111R/K112R mutants showed reduced transcriptional activity that was not responsive to p300 overexpression, while the K112R mutant retained activity. p300 and CBP were detected at the viral promoter; however, pCAF was not. We propose a model by which E2 transcriptional activity is controlled by p300-mediated acetylation of lysine 111. This model represents a novel mechanism regulating papillomavirus gene expression.

Indexed as

Gene Expression Regulation, ViralHost-Pathogen InteractionsTranscription, GeneticAcetylationAnimalsBovine papillomavirus 1CattleCell LineDNA-Binding ProteinsLysinep300-CBP-Associated Factorp300-CBP Transcription FactorsViral ProteinsDNA-Binding ProteinsE2 protein, Bovine papillomavirusLysinep300-CBP-Associated Factorp300-CBP Transcription FactorsViral Proteins

Identifiers

PMID23152516
PMCPMC3554136
OpenAlexW2026534551

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.