Evidence map›Paper›PMID 23376847›Full record

ArticleOncogene2014

p53 promotes repair of heterochromatin DNA by regulating JMJD2b and SUV39H1 expression.

H Zheng, L Chen, W J Pledger, J Fang, J Chen

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 66 citations in OpenAlex.

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  17. PHF2 histone demethylase prevents DNA damage and genome instability by controlling cell cycle progression of neural progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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.

H ZhengMolecular Oncology Department, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
L ChenMolecular Oncology Department, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
W J PledgerMolecular Oncology Department, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
J FangMolecular Oncology Department, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
J ChenMolecular Oncology Department, H. Lee Moffitt Cancer Center, Tampa, FL, USA.
Molecular Oncology (United States) · USMoffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Mechanisms of p53 activation during stress response (MPI)R01CA141244 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI JIANDONG CHEN, Gary W Daughdrill · 2009 to 2026
$5.3M
Function and Regulation of MDMXR01CA109636 · NCI · H. LEE MOFFITT CANCER CTR &RES INST · PI CHEN, JIANDONG · 2004 to 2014
$2.8M
NCI NIH HHS CA109636NCI NIH HHS CA141244NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA109636NCI NIH HHS R01 CA141244
6 · The paper itself

Abstract

Constitutive heterochromatin (HC) is important for maintaining chromosome stability, but also delays the repair of DNA double-strand breaks (DSBs). DSB repair in complex mammalian genomes involves a fast phase (2-6 h) in which most of the breaks are rapidly repaired, and a slow phase (up to 24 h) in which the remaining damages in HC are repaired. We found that p53 deficiency delays the slow-phase DNA repair after ionizing irradiation. p53 deficiency prevents downregulation of histone H3K9 trimethylation at the pericentric HC after DNA damage. Moreover, p53 directly induces expression of the H3K9 demethylase Jumonji domain 2 family demethylase (JMJD2b) through promoter binding. The p53 activation also indirectly downregulates expression of the H3K9 methyltransferase SUV39H1. Depletion of JMJD2b or sustained expression of SUV39H1 delays the repair of HC DNA and reduces clonogenic survival after ionizing irradiation. The results suggest that by regulating JMJD2b and SUV39H1 expression, p53 not only controls transcription but also promotes HC relaxation to accelerate a rate-limiting step in the repair of complex genomes.

Indexed as

DNA RepairCell Line, TumorDNA DamageDNA, NeoplasmHCT116 CellsHeterochromatinHumansJumonji Domain-Containing Histone DemethylasesMethyltransferasesRepressor ProteinsTransfectionTumor Suppressor Protein p53DNA, NeoplasmHeterochromatinJumonji Domain-Containing Histone DemethylasesKDM4B protein, humanMethyltransferasesRepressor ProteinsSUV39H1 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID23376847
PMCPMC3912226
OpenAlexW1983568365

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.