Evidence map›Paper›PMID 23979016›Full record

ArticleCell research2013

The mINO80 chromatin remodeling complex is required for efficient telomere replication and maintenance of genome stability.

Jin-Na Min, Yanyan Tian, Yang Xiao, Ling Wu, Lei Li, Sandy Chang

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2013. 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
3.6field-weighted citation impact, top 7% 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, 64 citations in OpenAlex.

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  10. Chromatin: the old and young of it.Frontiers in molecular biosciences · 2023
    Review
  11. Article
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  20. Epigenetics of Aging and Aging-Associated Diseases.International journal of molecular sciences · 2021
    Review
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

6 authors at 3 institutions in 1 country.

Jin-Na MinDepartment of Laboratory Medicine and Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.
Yanyan Tian
Yang Xiao
Ling Wu
Lei Li
Sandy Chang
Radiation Oncology Associates · USThe University of Texas MD Anderson Cancer Center · USYale University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Recognition and processing of complex lesions by components from multiple DNAP01CA097175 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI NAIRN, RODNEY S · 2004 to 2014
$15.3M
Telomere induced senescence as a supressor of tumorigenesisR01CA129037 · NCI · YALE UNIVERSITY · PI CHANG, SANDY S · 2007 to 2017
$3.1M
ATP-Dependent Chromatin Remodeling and Genomic Instability in Mammalian CellsR01CA127945 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, LEI · 2008 to 2013
$1.4M
NCI NIH HHS CA097175NCI NIH HHS CA127945NCI NIH HHS P01 CA097175NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA127945NCI NIH HHS R01 CA129037
6 · The paper itself

Abstract

The INO80 (inositol requiring mutant 80) chromatin remodeling complex plays important roles in transcriptional regulation and DNA replication and repair, and consists of several functional protein subunits, including the critical Ino80 ATPase catalytic subunit. While the function of INO80 has been studied in yeast and mammalian cell lines, we do not know how mIno80 contributes to the maintenance of genome stability to prevent cancer development in mice. Here, we use a conditional knockout approach to explore the cellular and organismal functions of mIno80. Deletion of mIno80 results in profound cellular proliferative defects and activation of p21-dependent cellular senescence. While mIno80 is required for efficient repair of DNA double strand breaks, its depletion did not impact upon the formation of γ-H2AX and 53BP1 DNA damage foci, or the activation of the ATM-CHK2-dependent DNA damage response. mIno80 deletion inhibited the generation of single-strand DNA, resulting in defects in homology-directed DNA repair (HDR) at telomeres. Fragile telomeres were prominent in mIno80(Δ/Δ) MEFs, suggesting that chromatin remodeling is required for efficient telomere replication. mIno80(-/-) mouse embryos die early during embryogenesis, while conditional deletion of mIno80 in adult mice results in weight loss and premature death. In a p53(-/-) tumor-prone background, mIno80 haploinsufficiency favored the development of sarcomas. Our studies suggest that the mIno80 chromatin remodeling complex plays important roles in telomere replication, HDR-mediated repair of dysfunctional telomeres, and maintenance of genome stability.

Indexed as

Genomic InstabilityAllelesAnimalsCells, CulturedCellular SenescenceChromatinChromatin Assembly and DisassemblyDNA Breaks, Double-StrandedDNA HelicasesDNA RepairDNA ReplicationFibroblastsHydroxyureaMiceMice, Inbred C57BLMice, KnockoutChromatinDNA HelicasesHydroxyureaNucleic Acid Synthesis InhibitorsTumor Suppressor Protein p53

Identifiers

PMID23979016
PMCPMC3847565
OpenAlexW1992418320

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.