Evidence map›Paper›PMID 37219458›Full record

ArticleJournal of virology2023

Targeting Cell Cycle Facilitates E1A-Independent Adenoviral Replication.

Maximilian Ehrenfeld, Felicia Segeth, Klaus Mantwill, Corinna Brockhaus, Yuling Zhao, Christian Ploner, Andreas Kolk, Jürgen E Gschwend, Roman Nawroth, Per Sonne Holm

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2023. 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
4.4field-weighted citation impact, top 5% 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, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Flavonoid compound fromFrontiers in cellular and infection microbiology · 2025
    Article
  4. Article
  5. Review
  6. Review
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.

Maximilian Ehrenfeld *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Felicia Segeth *Department of Oral and Maxillofacial Surgery, Medical University of Innsbruck, Innsbruck, Austria.
Klaus Mantwill *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Corinna Brockhaus *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Yuling Zhao *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Christian Ploner *Department of Plastic, Reconstructive and Aesthetic Surgery, Medical University of Innsbruck, Innsbruck, Austria.
Andreas Kolk *Department of Oral and Maxillofacial Surgery, Medical University of Innsbruck, Innsbruck, Austria.
Jürgen E Gschwend *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Roman Nawroth *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Per Sonne Holm *Department of Urology, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.ORCID 0000-0002-1196-2323
TUM Klinikum · DEInnsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA replication of E1-deleted first-generation adenoviruses (AdV) in cultured cancer cells has been reported repeatedly and it was suggested that certain cellular proteins could functionally compensate for E1A, leading to the expression of the early region 2 (E2)-encoded proteins and subsequently virus replication. Referring to this, the observation was named E1A-like activity. In this study, we investigated different cell cycle inhibitors with respect to their ability to increase viral DNA replication of dl70-3, an E1-deleted adenovirus. Our analyses of this issue revealed that in particular inhibition of cyclin-dependent kinases 4/6 (CDK4/6i) increased E1-independent adenovirus E2-expression and viral DNA replication. Detailed analysis of the E2-expression in dl70-3 infected cells by RT-qPCR showed that the increase in E2-expression originated from the E2-early promoter. Mutations of the two E2F-binding sites in the E2-early promoter (pE2early-LucM) caused a significant reduction in E2-early promoter activity in

Indexed as

AdenoviridaeCell CycleDNA ReplicationVirus ReplicationAdenovirus E1A ProteinsBinding SitesCell Line, TumorCellsDNA, ViralGene Expression Regulation, ViralHumansMutationPromoter Regions, GeneticProtein Kinase InhibitorsAdenovirus E1A ProteinsDNA, ViralProtein Kinase InhibitorsadenovirusCDK4/6cell cycleE1AE2Fnutlin-3aRbribociclibYB-1

Identifiers

PMID37219458
PMCPMC10308897
OpenAlexW4377564840

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.