Evidence map›Paper›PMID 24994062›Full record

ArticleDNA repair2014

Repair of endogenous DNA base lesions modulate lifespan in mice.

Lisiane B Meira, Jennifer A Calvo, Dharini Shah, Joanna Klapacz, Catherine A Moroski-Erkul, Roderick T Bronson, Leona D Samson

Abstract read
In one paragraph

Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.9field-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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Germline Predisposition to Oncogenic Alkylating Damage in Colorectal Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

7 authors at 2 institutions in 1 country.

Lisiane B MeiraBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States.
Jennifer A CalvoBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States.
Dharini ShahBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States.
Joanna KlapaczBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States.
Catherine A Moroski-ErkulBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States.
Roderick T BronsonKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Rodent Histopathology Core, Harvard Medical School, 126 Goldenson Building, Boston, MA 02115, United States.
Leona D SamsonBiological Engineering Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Biology Department, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Center for Environmental Health Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States; Rodent Histopathology Core, Harvard Medical School, 126 Goldenson Building, Boston, MA 02115, United States. Electronic address: lsamson@mit.edu.
Center for Environmental Health · USHarvard University · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
IN VIVO ROLE OF DNA ALKYLATION REPAIRR01CA075576 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1997 to 2011
$4.9M
EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
Eukaryotic DNA Alkylation RepairR01ES022872 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2013 to 2017
$1.7M
The influence of DNA repair on inflammation associated carcinogenesisR01CA149261 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2010 to 2014
$1.7M
NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NCI NIH HHS R01 CA055042NCI NIH HHS R01 CA075576NCI NIH HHS R01-CA075576NCI NIH HHS R01 CA149261NCI NIH HHS R01-CA149261NIEHS NIH HHS P30 ES002109NIEHS NIH HHS P30-ES002109NIEHS NIH HHS R01 ES022872NIEHS NIH HHS R01-ES022872
6 · The paper itself

Abstract

The accumulation of DNA damage is thought to contribute to the physiological decay associated with the aging process. Here, we report the results of a large-scale study examining longevity in various mouse models defective in the repair of DNA alkylation damage, or defective in the DNA damage response. We find that the repair of spontaneous DNA damage by alkyladenine DNA glycosylase (Aag/Mpg)-initiated base excision repair and O(6)-methylguanine DNA methyltransferase (Mgmt)-mediated direct reversal contributes to maximum life span in the laboratory mouse. We also uncovered important genetic interactions between Aag, which excises a wide variety of damaged DNA bases, and the DNA damage sensor and signaling protein, Atm. We show that Atm plays a role in mediating survival in the face of both spontaneous and induced DNA damage, and that Aag deficiency not only promotes overall survival, but also alters the tumor spectrum in Atm(-/-) mice. Further, the reversal of spontaneous alkylation damage by Mgmt interacts with the DNA mismatch repair pathway to modulate survival and tumor spectrum. Since these aging studies were performed without treatment with DNA damaging agents, our results indicate that the DNA damage that is generated endogenously accumulates with age, and that DNA alkylation repair proteins play a role in influencing longevity.

Indexed as

DNA RepairAnimalsAtaxia Telangiectasia Mutated ProteinsDNA GlycosylasesDNA Modification MethylasesDNA Repair EnzymesLongevityMiceMice, Inbred C57BLTumor Suppressor Proteins3-methyladenine-DNA glycosylaseAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseDNA GlycosylasesDNA Modification MethylasesDNA Repair EnzymesMGMT protein, mouseTumor Suppressor ProteinsAAG/MPGAgingBase excision repairDNA adductsDNA glycosylaseMgmt

Identifiers

PMID24994062
PMCPMC4125484
OpenAlexW2011675522

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.