Evidence map›Paper›PMID 25957489›Full record

ReviewDNA repair2015

Preventing replication fork collapse to maintain genome integrity.

David Cortez

Abstract readReview
In one paragraph

Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
–field-weighted citation impact
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

139 citing papers in PubMed.

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79 more citing papers are in PubMed but not listed here.

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

1 author.

David CortezDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37027, USA. Electronic address: david.cortez@vanderbilt.edu.

Funding

Function of the ATR-ATRIP ComplexR01CA102729 · NCI · VANDERBILT UNIVERSITY · PI CORTEZ, DAVID K · 2003 to 2018
$4.2M
NCI NIH HHS R01 CA102729NCI NIH HHS R01CA102729
6 · The paper itself

Abstract

Billions of base pairs of DNA must be replicated trillions of times in a human lifetime. Complete and accurate replication once and only once per cell division cycle is essential to maintain genome integrity and prevent disease. Impediments to replication fork progression including difficult to replicate DNA sequences, conflicts with transcription, and DNA damage further add to the genome maintenance challenge. These obstacles frequently cause fork stalling, but only rarely cause a failure to complete replication. Robust mechanisms ensure that stalled forks remain stable and capable of either resuming DNA synthesis or being rescued by converging forks. However, when failures do happen the fork collapses leading to genome rearrangements, cell death and disease. Despite intense interest, the mechanisms to repair damaged replication forks, stabilize them, and ensure successful replication remain only partly understood. Different models of fork collapse have been proposed with varying descriptions of what happens to the DNA and replisome. Here, I will define fork collapse and describe what is known about how the replication checkpoint prevents it to maintain genome stability.

Indexed as

DNA RepairDNA ReplicationGenomic InstabilityAnimalsDNADNA DamageDNA Polymerase IIIGene Expression RegulationHumansMiceProliferating Cell Nuclear AntigenSaccharomyces cerevisiaeXenopus laevisDNADNA Polymerase IIIProliferating Cell Nuclear AntigenATRFork collapseiPONDReplication checkpointReplisome

Identifiers

PMID25957489
PMCPMC4522347

What OpenQuestion holds

Textmetadata
LicenceTDM
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.