Evidence map›Paper›PMID 11285218›Full record

ArticleThe EMBO journal2001

Elevated Cu/Zn-SOD exacerbates radiation sensitivity and hematopoietic abnormalities of Atm-deficient mice.

Y Peter, G Rotman, J Lotem, A Elson, Y Shiloh, Y Groner

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
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  6. Stem cells, redox signaling, and stem cell aging.Antioxidants & redox signaling · 2014
    Review
  7. Reducing mitochondrial ROS improves disease-related pathology in a mouse model of ataxia-telangiectasia.Molecular therapy : the journal of the American Society of Gene Therapy · 2013
    Article
  8. Article
  9. Article
  10. Article
  11. Review
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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

6 authors at 1 institution in 1 country.

Y PeterDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100.
G Rotman
J Lotem
A Elson
Y Shiloh
Y Groner
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with the genetic disorder ataxia-telangiectasia (A-T) display a pleiotropic phenotype that includes neurodegeneration, immunodeficiency, cancer predisposition and hypersensitivity to ionizing radiation. The gene responsible is ATM, and ATM:-knockout mice recapitulate most features of A-T. In order to study the involvement of oxidative stress in the A-T phenotype, we examined mice deficient for Atm and overexpressing human Cu/Zn superoxide dismutase (SOD1). We report that elevated levels of SOD1 exacerbate specific features of the murine Atm- deficient phenotype, including abnormalities in hematopoiesis and radiosensitivity. The data are consistent with the possibility that oxidative stress contributes to some of the clinical features associated with the A-T phenotype.

Indexed as

HematopoiesisRadiation ToleranceAnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCerebellumDisease Models, AnimalDNA-Binding ProteinsFemaleGrowth DisordersHumansKidneyLiverMaleMiceAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Tumor Suppressor Proteins

Identifiers

PMID11285218
PMCPMC145498
OpenAlexW2046568492

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.