Evidence map›Paper›PMID 22869592›Full record

ArticleThe Journal of cell biology2012

The ATM protein: the importance of being active.

Yosef Shiloh, Yael Ziv

Open access · bronzeAbstract readComment
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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  11. Sensing Bacterial-Induced DNA Damaging EffectsFrontiers in immunology · 2018
    Review
  12. Genomically amplified Akt3 activates DNA repair pathway and promotes glioma progression.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Article
  14. Article
  15. Tug of war between survival and death: exploring ATM function in cancer.International journal of molecular sciences · 2014
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yosef ShilohThe David and Inez Myers Laboratory for Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. yossih@post.tau.ac.il
Yael Ziv
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics.

Indexed as

Gene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicMutationAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsFemaleHumansProtein Serine-Threonine KinasesTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID22869592
PMCPMC3413363
OpenAlexW2107175043

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.