Evidence map›Paper›PMID 23135708›Full record

ArticleJournal of virology2013

The adenoviral oncogene E1A-13S interacts with a specific isoform of the tumor suppressor PML to enhance viral transcription.

Julia Berscheminski, Peter Groitl, Thomas Dobner, Peter Wimmer, Sabrina Schreiner

Open access · bronzeAbstract 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 38 citations in OpenAlex.

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  13. Negri bodies and other virus membrane-less replication compartments.Biochimica et biophysica acta. Molecular cell research · 2020
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  16. The Role of Promyelocytic Leukemia Nuclear Bodies During HPV Infection.Frontiers in cellular and infection microbiology · 2020
    Review
  17. 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 1 institution in 1 country.

Julia BerscheminskiHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.
Peter Groitl
Thomas Dobner
Peter Wimmer
Sabrina Schreiner
Leibniz Institute of Virology (LIV) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PML nuclear bodies (PML NBs), also called ND10, are matrix-bound nuclear structures that have been implicated in a variety of functions, including DNA repair, transcriptional regulation, protein degradation, and tumor suppression. These domains are also known for their potential to mediate an intracellular defense mechanism against many virus types. This is likely why they are targeted and subsequently manipulated by numerous viral proteins. Paradoxically, the genomes of various DNA viruses become associated with PML NBs, and initial sites of viral transcription/replication centers are often juxtaposed to these domains. The question is why viruses start their transcription and replication next to their supposed antagonists. Here, we report that PML NBs are targeted by the adenoviral (Ad) transactivator protein E1A-13S. Alternatively spliced E1A isoforms (E1A-12S and E1A-13S) are the first proteins expressed upon Ad infection. E1A-13S is essential for activating viral transcription in the early phase of infection. Coimmunoprecipitation assays showed that E1A-13S preferentially interacts with only one (PML-II) of at least six nuclear human PML isoforms. Deletion mapping located the interaction site within E1A conserved region 3 (CR3), which was previously described as the transcription factor binding region of E1A-13S. Indeed, cooperation with PML-II enhanced E1A-mediated transcriptional activation, while deleting the SUMO-interacting motif (SIM) of PML proved even more effective. Our results suggest that in contrast to PML NB-associated antiviral defense, PML-II may help transactivate viral gene expression and therefore play a novel role in activating Ad transcription during the early viral life cycle.

Indexed as

Host-Pathogen InteractionsTranscription, GeneticAdenovirus E1A ProteinsAdenoviruses, HumanBinding SitesDNA Mutational AnalysisHumansImmunoprecipitationNuclear ProteinsPromyelocytic Leukemia ProteinProtein BindingProtein Interaction MappingProtein IsoformsSequence DeletionTranscription FactorsTumor Suppressor ProteinsAdenovirus E1A ProteinsNuclear ProteinsPML protein, humanPromyelocytic Leukemia ProteinProtein IsoformsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID23135708
PMCPMC3554061
OpenAlexW2089237129

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.