Evidence map›Paper›PMID 23740993›Full record

ArticleJournal of virology2013

Adenovirus E1A oncogene induces rereplication of cellular DNA and alters DNA replication dynamics.

Ghata Singhal, Elisabetta Leo, Saayi Krushna Gadham Setty, Yves Pommier, Bayar Thimmapaya

Registry-linked trialOpen 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. It is linked to trial NCT03325517 (Effect of Adenovirus E1A Oncogene on DNA Replication Dynamics), which is not on this map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 24% 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.

NCT03325517 unknown statusnot on this mapstarted 2017, after this paper: background citation

Effect of Adenovirus E1A Oncogene on DNA Replication Dynamics

TypeobservationalSponsorHeba Momen kamelRan2017 to 2019Enrolled50ConditionsAdenovirus
3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 17 citations in OpenAlex.

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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 2 institutions in 1 country.

Ghata SinghalMicrobiology and Immunology Department, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Elisabetta Leo
Saayi Krushna Gadham Setty
Yves Pommier
Bayar Thimmapaya
Northwestern University · USNational Cancer Institute · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
FUNCTIONS OF AN EIA-ASSOCIATED CELLULAR PROTEINR01CA074403 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THIMMAPAYA, BAYAR · 1998 to 2010
$2.8M
E1A Oncoprotein Induced Deregulation of Replication Origin FiringR21AI094296 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THIMMAPAYA, BAYAR · 2011 to 2012
$419k
Intramural NIH HHSNCI NIH HHS CA060553NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA074403NCI NIH HHS R01CA 74403NIAID NIH HHS R21 AI094296NIAID NIH HHS R21AI094296
6 · The paper itself

Abstract

The oncogenic property of the adenovirus (Ad) transforming E1A protein is linked to its capacity to induce cellular DNA synthesis which occurs as a result of its interaction with several host proteins, including pRb and p300/CBP. While the proteins that contribute to the forced induction of cellular DNA synthesis have been intensively studied, the nature of the cellular DNA replication that is induced by E1A in quiescent cells is not well understood. Here we show that E1A expression in quiescent cells leads to massive cellular DNA rereplication in late S phase. Using a single-molecule DNA fiber assay, we studied the cellular DNA replication dynamics in E1A-expressing cells. Our studies show that the DNA replication pattern is dramatically altered in E1A-expressing cells, with increased replicon length, fork velocity, and interorigin distance. The interorigin distance increased by about 3-fold, suggesting that fewer DNA replication origins are used in E1A-expressing cells. These aberrant replication events led to replication stress, as evidenced by the activation of the DNA damage response. In earlier studies, we showed that E1A induces c-Myc as a result of E1A binding to p300. Using an antisense c-Myc to block c-Myc expression, our results indicate that induction of c-Myc in E1A-expressing cells contributes to the induction of host DNA replication. Together, our results suggest that the E1A oncogene-induced cellular DNA replication stress is due to dramatically altered cellular replication events and that E1A-induced c-Myc may contribute to these events.

Indexed as

DNA ReplicationHost-Pathogen InteractionsAdenoviridaeAdenovirus E1A ProteinsCarcinogensCell LineGene Expression ProfilingHumansMicroarray AnalysisProto-Oncogene Proteins c-mycAdenovirus E1A ProteinsCarcinogensMYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID23740993
PMCPMC3719816
OpenAlexW2068083438

What OpenQuestion holds

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Registered trials

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.