Evidence map›Paper›PMID 30469473›Full record

ArticleViruses2018

The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.

Ali Zhang, Tanner M Tessier, Kristianne J C Galpin, Cason R King, Steven F Gameiro, Wyatt W Anderson, Ahmed F Yousef, Wen T Qin, Shawn S C Li, Joe S Mymryk

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. ZMYND11 Restrains KMT2A to Enable a Neuronal Developmental Program.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
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

10 authors at 2 institutions in 2 countries.

Ali ZhangDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. azhang44@uwo.ca.
Tanner M TessierDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. ttessie2@uwo.ca.
Kristianne J C GalpinDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. kgalpin@ohri.ca.ORCID 0000-0002-4199-6874
Cason R KingDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. cking46@uwo.ca.ORCID 0000-0002-5531-5347
Steven F GameiroDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. sgameiro@uwo.ca.
Wyatt W AndersonDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. wander@uwo.ca.
Ahmed F YousefDepartment of Chemistry, Khalifa University, 54224 Abu Dhabi, UAE. ahmed.yousef@ku.ac.ae.
Wen T QinDepartment of Biochemistry, The University of Western Ontario, London, ON N6A 3K7, Canada. wqin24@uwo.ca.ORCID 0000-0002-0636-8506
Shawn S C LiDepartment of Biochemistry, The University of Western Ontario, London, ON N6A 3K7, Canada. sli@uwo.ca.
Joe S MymrykDepartment of Microbiology and Immunology, The University of Western Ontario, London, ON N6A 3K7, Canada. jmymryk@uwo.ca.
Western University · CAKhalifa University of Science and Technology · AE

Funding

CIHR MOP-148689
6 · The paper itself

Abstract

Early region 1A (E1A) is the first viral protein produced upon human adenovirus (HAdV) infection. This multifunctional protein transcriptionally activates other HAdV early genes and reprograms gene expression in host cells to support productive infection. E1A functions by interacting with key cellular regulatory proteins through short linear motifs (SLiMs). In this study, the molecular determinants of interaction between E1A and BS69, a cellular repressor that negatively regulates E1A transactivation, were systematically defined by mutagenesis experiments. We found that a minimal sequence comprised of MPNLVPEV, which contains a conserved PXLXP motif and spans residues 112⁻119 in HAdV-C5 E1A, was necessary and sufficient in binding to the myeloid, Nervy, and DEAF-1 (MYND) domain of BS69. Our study also identified residues P113 and L115 as critical for this interaction. Furthermore, the HAdV-C5 and -A12 E1A proteins from species C and A bound BS69, but those of HAdV-B3, -E4, -D9, -F40, and -G52 from species B, E, D, F, and G, respectively, did not. In addition, BS69 functioned as a repressor of E1A-mediated transactivation, but only for HAdV-C5 and HAdV-A12 E1A. Thus, the PXLXP motif present in a subset of HAdV E1A proteins confers interaction with BS69, which serves as a negative regulator of E1A mediated transcriptional activation.

Indexed as

Binding SitesGene Expression Regulation, ViralAdenovirus E1A ProteinsAdenoviruses, HumanAmino Acid MotifsAmino Acid SequenceCarrier ProteinsCell Cycle ProteinsCell Line, TumorConserved SequenceCo-Repressor ProteinsDNA-Binding ProteinsGene ExpressionGenes, ReporterGenotypeHumansAdenovirus E1A ProteinsCarrier ProteinsCell Cycle ProteinsCo-Repressor ProteinsDNA-Binding ProteinsTranscription FactorsZMYND11 protein, humanBS69E1Ahuman adenovirusshort linear motifstranscriptional regulationZMYND11

Identifiers

PMID30469473
PMCPMC6315623
OpenAlexW2901150554

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.