Evidence map›Paper›PMID 27174871›Full record

ReviewActa biochimica et biophysica Sinica2016

Sharpening the ends for repair: mechanisms and regulation of DNA resection.

Sharad C Paudyal, Zhongsheng You

Abstract readReview
In one paragraph

Review in Acta biochimica et biophysica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. ATM controls the extent of DNA end resection by eliciting sequential posttranslational modifications of CtIP.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Article
  6. Article
  7. Article
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

2 authors.

Sharad C PaudyalDepartment of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA.
Zhongsheng YouDepartment of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA zyou@wustl.edu.

Funding

MOLECULAR MECHANISMS OF DNA DAMAGE SIGNALING AND REPAIRR01GM098535 · NIGMS · WASHINGTON UNIVERSITY · PI PISTON, DAVID W · 2012 to 2025
$4.2M
NIGMS NIH HHS R01 GM098535
6 · The paper itself

Abstract

DNA end resection is a key process in the cellular response to DNA double-strand break damage that is essential for genome maintenance and cell survival. Resection involves selective processing of 5' ends of broken DNA to generate ssDNA overhangs, which in turn control both DNA repair and checkpoint signaling. DNA resection is the first step in homologous recombination-mediated repair and a prerequisite for the activation of the ataxia telangiectasia mutated and Rad3-related (ATR)-dependent checkpoint that coordinates repair with cell cycle progression and other cellular processes. Resection occurs in a cell cycle-dependent manner and is regulated by multiple factors to ensure an optimal amount of ssDNA required for proper repair and genome stability. Here, we review the latest findings on the molecular mechanisms and regulation of the DNA end resection process and their implications for cancer formation and treatment.

Indexed as

DNA RepairDNA Breaks, Double-StrandedDNA ReplicationDNA, Single-StrandedHeterochromatinTelomereDNA, Single-StrandedHeterochromatincancerDNA damage responseDNA end resectionExo1MRN-CtIP

Identifiers

PMID27174871
PMCPMC4930117

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.