Evidence map›Paper›PMID 22869596›Full record

ArticleThe Journal of cell biology2012

Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice.

Kenta Yamamoto, Yunyue Wang, Wenxia Jiang, Xiangyu Liu, Richard L Dubois, Chyuan-Sheng Lin, Thomas Ludwig, Christopher J Bakkenist, Shan Zha

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
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  10. Cancer Cells Haploinsufficient for ATM Are Sensitized to PARP Inhibitors byInternational journal of molecular sciences · 2022
    Article
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  20. It takes three to the DNA damage response tango.Molecular & cellular oncology · 2021
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Kenta YamamotoInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Yunyue Wang
Wenxia Jiang
Xiangyu Liu
Richard L Dubois
Chyuan-Sheng Lin
Thomas Ludwig
Christopher J Bakkenist
Shan Zha
Columbia University · USColumbia University Irving Medical Center · USHerbert Irving Comprehensive Cancer CenterUPMC Hillman Cancer Center · US

Funding

CELL, MOLECULAR AND DEVELOPMENTAL BIOLOGY OF CANCERT32CA009503 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GAUTIER, JEAN · 1985 to 2016
$6.8M
The role of ATM in the suppression of lymphoid malignancyR01CA158073 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Shan Zha · 2011 to 2026
$5.7M
DNA-PKCS Phosphorylation in DNA Repair and Chromosomal TranslocationsR01CA184187 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ZHA, SHAN · 2015 to 2019
$1.8M
Regulation of DNA replication fork progression by ATM kinase activityR01CA148644 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAKKENIST, CHRISTOPHER J. · 2011 to 2015
$1.3M
NCI NIH HHS CA148644NCI NIH HHS CA158073NCI NIH HHS R01 CA148644NCI NIH HHS R01 CA158073NCI NIH HHS R01 CA184187NCI NIH HHS T32 CA009503NCI NIH HHS T32-CA09503
6 · The paper itself

Abstract

Ataxia telangiectasia (A-T) mutated (ATM) kinase orchestrates deoxyribonucleic acid (DNA) damage responses by phosphorylating numerous substrates implicated in DNA repair and cell cycle checkpoint activation. A-T patients and mouse models that express no ATM protein undergo normal embryonic development but exhibit pleiotropic DNA repair defects. In this paper, we report that mice carrying homozygous kinase-dead mutations in Atm (Atm(KD/KD)) died during early embryonic development. Atm(KD/-) cells exhibited proliferation defects and genomic instability, especially chromatid breaks, at levels higher than Atm(-/-) cells. Despite this increased genomic instability, Atm(KD/-) lymphocytes progressed through variable, diversity, and joining recombination and immunoglobulin class switch recombination, two events requiring nonhomologous end joining, at levels comparable to Atm(-/-) lymphocytes. Together, these results reveal an essential function of ATM during embryogenesis and an important function of catalytically inactive ATM protein in DNA repair.

Indexed as

Gene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicAllelesAnimalsAtaxia Telangiectasia Mutated ProteinsBase SequenceCatalysisCell Cycle ProteinsDNA-Binding ProteinsDNA DamageDNA RepairExonsFemaleHomozygoteHumansLymphocytesAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID22869596
PMCPMC3413350
OpenAlexW2105719362

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.