Evidence map›Paper›PMID 20179206›Full record

ArticleCancer research2010

Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.

Aya M Westbrook, Robert H Schiestl

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. Dendritic cells in inborn errors of immunity.Frontiers in immunology · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Accumulation of Cytoplasmic DNA Due to ATM Deficiency Activates the Microglial Viral Response System with Neurotoxic Consequences.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  14. Article
  15. Article
  16. Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
  17. Review
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Aya M WestbrookMolecular Toxicology Interdepartmental Program, University of California at Los Angeles School of Medicine, Los Angeles, California 90095, USA.
Robert H Schiestl
University of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Training in Molecular ToxicologyT32ES015457 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALLARD, PATRICK, HANKINSON, OLIVER NMN · 2008 to 2025
$4.0M
ATM, P53, GADD45 AND P21 EFFECTS ON RECOMBINATIONR01ES009519 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SCHIESTL, ROBERT H · 1999 to 2009
$2.7M
NCI NIH HHS CA016042NCI NIH HHS P30 CA016042NIEHS NIH HHS ES09519NIEHS NIH HHS R01 ES009519NIEHS NIH HHS T32 ES015457
6 · The paper itself

Abstract

The role of ataxia telangiectasia mutated (ATM), a DNA double-strand break recognition and response protein, in inflammation and inflammatory diseases is unclear. We have previously shown that high levels of systemic DNA damage are induced by intestinal inflammation in wild-type mice. To determine the effect of Atm deficiency in inflammation, we induced experimental colitis in Atm(-/-), Atm(+/-), and wild-type mice via dextran sulfate sodium (DSS) administration. Atm(-/-) mice had higher disease activity indices and rates of mortality compared with heterozygous and wild-type mice. Systemic DNA damage and immune response were characterized in peripheral blood throughout and after three cycles of treatment. Atm(-/-) mice showed increased sensitivity to levels of DNA strand breaks in peripheral leukocytes, as well as micronucleus formation in erythroblasts, compared with heterozygous and wild-type mice, especially during remission periods and after the end of treatment. Markers of reactive oxygen and nitrogen species-mediated damage, including 8-oxoguanine and nitrotyrosine, were present both in the distal colon and in peripheral leukocytes, with Atm(-/-) mice manifesting more 8-oxoguanine formation than wild-type mice. Atm(-/-) mice showed greater upregulation of inflammatory cytokines and significantly higher percentages of activated CD69+ and CD44+ T cells in the peripheral blood throughout treatment. ATM, therefore, may be a critical immunoregulatory factor dampening the deleterious effects of chronic DSS-induced inflammation, necessary for systemic genomic stability and homeostasis of the gut epithelial barrier.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsColitisColonCytokinesDextran SulfateDNA-Binding ProteinsGuanineMiceMice, Inbred C57BLMice, TransgenicProtein Serine-Threonine KinasesT-LymphocytesTumor Suppressor Proteins8-hydroxyguanineAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsCytokinesDextran SulfateDNA-Binding ProteinsGuanineProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID20179206
PMCPMC2831166
OpenAlexW2143557924

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.