Evidence map›Paper›PMID 33665206›Full record

ReviewFrontiers in molecular biosciences2020

E2F1: Cause and Consequence of DNA Replication Stress.

Shahd Fouad, David Hauton, Vincenzo D'Angiolella

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.0field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Dysregulation of Aurora Kinases andCurrent issues in molecular biology · 2026
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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

3 authors at 3 institutions in 1 country.

Shahd FouadDepartment of Oncology, Medical Research Council Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom.
David HautonDepartment of Oncology, Medical Research Council Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom.
Vincenzo D'AngiolellaDepartment of Oncology, Medical Research Council Oxford Institute for Radiation Oncology, University of Oxford, Oxford, United Kingdom.
CRUK/MRC Oxford Institute for Radiation Oncology · GBMedical Research Council · GBUniversity of Oxford · GB

Funding

Medical Research Council MC_UU_00001/7
6 · The paper itself

Abstract

In mammalian cells, cell cycle entry occurs in response to the correct stimuli and is promoted by the transcriptional activity of E2F family members. E2F proteins regulate the transcription of S phase cyclins and genes required for DNA replication, DNA repair, and apoptosis. The activity of E2F1, the archetypal and most heavily studied E2F family member, is tightly controlled by the DNA damage checkpoints to modulate cell cycle progression and initiate programmed cell death, when required. Altered tumor suppressor and oncogenic signaling pathways often result in direct or indirect interference with E2F1 regulation to ensure higher rates of cell proliferation independently of external cues. Despite a clear link between dysregulated E2F1 activity and cancer progression, literature on the contribution of E2F1 to DNA replication stress phenotypes is somewhat scarce. This review discusses how dysfunctional tumor suppressor and oncogenic signaling pathways promote the disruption of E2F1 transcription and hence of its transcriptional targets, and how such events have the potential to drive DNA replication stress. In addition to the involvement of E2F1 upstream of DNA replication stress, this manuscript also considers the role of E2F1 as a downstream effector of the response to this type of cellular stress. Lastly, the review introduces some reflections on how E2F1 activity is integrated with checkpoint control through post-translational regulation, and proposes an exploitable tumor weakness based on this axis.

Indexed as

cyclin Ecyclin FDNA replication stressE2F1retinoblastomaribonucleotide reductaseubiquitin proteasome system

Identifiers

PMID33665206
PMCPMC7921158
OpenAlexW3133052187

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.