Evidence map›Paper›PMID 26440899›Full record

ArticleCell reports2015

ATM Dependent Silencing Links Nucleolar Chromatin Reorganization to DNA Damage Recognition.

Shane M Harding, Jonathan A Boiarsky, Roger A Greenberg

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 186 citations in OpenAlex.

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54 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

3 authors at 2 institutions in 1 country.

Shane M HardingDepartments of Cancer Biology and Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
Jonathan A BoiarskyDepartments of Cancer Biology and Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
Roger A GreenbergDepartments of Cancer Biology and Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA. Electronic address: rogergr@mail.med.upenn.edu.
Cancer Research Institute · USUniversity of Pennsylvania · US

Funding

The RAP80-BRCC36 Deubiquitinating Complex in DNA RepairR01CA138835 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Roger A Greenberg · 2010 to 2026
$5.2M
Roles of Chromatin Modification in BRCA1 Dependent DNA RepairR01CA174904 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Roger A Greenberg · 2013 to 2026
$4.8M
DNA Double Strand Break Chromatin Alterations and Genome IntegrityR01GM101149 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GREENBERG, ROGER A · 2013 to 2025
$4.0M
NCI NIH HHS CA138835NCI NIH HHS CA17494NCI NIH HHS R01 CA138835NCI NIH HHS R01 CA174904NIGMS NIH HHS GM101149NIGMS NIH HHS R01 GM101149
6 · The paper itself

Abstract

Resolution of DNA double-strand breaks (DSBs) is essential for the suppression of genome instability. DSB repair in transcriptionally active genomic regions represents a unique challenge that is associated with ataxia telangiectasia mutated (ATM) kinase-mediated transcriptional silencing. Despite emerging insights into the underlying mechanisms, how DSB silencing connects to DNA repair remains undefined. We observe that silencing within the rDNA depends on persistent DSBs. Non-homologous end-joining was the predominant mode of DSB repair allowing transcription to resume. ATM-dependent rDNA silencing in the presence of persistent DSBs led to the large-scale reorganization of nucleolar architecture, with movement of damaged chromatin to nucleolar cap regions. These findings identify ATM-dependent temporal and spatial control of DNA repair and provide insights into how communication between DSB signaling and ongoing transcription promotes genome integrity.

Indexed as

DNA Breaks, Double-StrandedGene SilencingAnimalsAtaxia Telangiectasia Mutated ProteinsCell LineCell NucleolusChromatinDNA End-Joining RepairHumansMCF-7 CellsMiceTranscription, GeneticAtaxia Telangiectasia Mutated ProteinsATM protein, humanChromatin

Identifiers

PMID26440899
PMCPMC4607662
OpenAlexW2124418183

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.