Evidence map›Paper›PMID 19071232›Full record

ArticleDNA repair2009

No attenuation of the ATM-dependent DNA damage response in murine telomerase-deficient cells.

Natalie Erdmann, Lea A Harrington

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Transient induction of telomerase expression mediates senescence and reduces tumorigenesis in primary fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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.

Natalie ErdmannDepartment of Medical Biophysics, Ontario Cancer Institute and Campbell Family Institute for Breast Cancer Research, University of Toronto, Toronto, ON, Canada.
Lea A Harrington
University of Toronto · CA

Funding

A unique murine model for human agingR01AG024398 · NIA · UNIVERSITY HEALTH NETWORK · PI HARRINGTON, LEA A · 2004 to 2008
$1.4M
GENETIC ANALYSIS OF MAMMALIAN TELOMERASE PROTEINS TEP1R01AG016629 · NIA · ONTARIO CANCER INSTITUTE · PI HARRINGTON, LEA A. · 1999 to 2003
$646k
AGING, DISEASE, AND DRUGS ON DIGITALIS SENSITIVITYR01AG002398 · NIA · MICHIGAN STATE UNIVERSITY · PI BRODY, THEODORE M. · 1985 to 1988
–
Howard Hughes Medical Institute HHMI 55005945NIA NIH HHS R01 AG016629NIA NIH HHS R01 AG02398NIA NIH HHS R01 AG024398
6 · The paper itself

Abstract

Inactivation of mammalian telomerase leads to telomere attrition, eventually culminating in uncapped telomeres, which elicit a DNA damage response and cell cycle arrest or death. In some instances, telomerase modulation evokes a response not obviously attributable to changes in telomere length. One such example is the suppression of the DNA damage response (DDR) and changes in histone modification that occur upon repression of the telomerase reverse transcriptase, TERT, in human primary cells [K. Masutomi, R. Possemato, J.M. Wong, J.L. Currier, Z. Tothova, J.B. Manola, S. Ganesan, P.M. Lansdorp, K. Collins and W.C. Hahn, The telomerase reverse transcriptase regulates chromatin state and DNA damage responses, Proc. Natl. Acad. Sci. U.S.A. 102 (2005) 8222-8227]. Here, we evaluate the contribution of TERT to the DDR in murine Tert(-/-) cells without critically shortened telomeres. We treated mTert(-/-) embryonic stem (ES) cells and murine embryonic fibroblasts (MEFs) with etoposide and irradiation, and assessed the status of p53(pS15), 53BP1, ATM(pS1981), SMC1(pS957), and gammaH2AX by indirect immunofluorescence or western blotting. In four independently derived mTert(-/-) ES cell lines, there was no significant difference in the induction of gammaH2AX, 53BP1 foci, or the phosphorylation of ATM targets (ATM, SMC1, p53) between wildtype and mTert(-/-) ES cells and MEFs. A slight difference in post-translational modification of histones H3 and H4 was observed in a subset of mTert(-/-) ES cells, however this difference was reflected in the cellular levels of H3 and H4. Thus, in contrast to previous studies in human cells, the absence of Tert does not overtly affect the ATM-dependent response to DNA damage in murine cells.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsBlotting, WesternCell Cycle ProteinsCell LineChromosomal Proteins, Non-HistoneDNA-Binding ProteinsFluorescent Antibody Technique, IndirectHistonesIntracellular Signaling Peptides and ProteinsMicePhosphorylationProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesStructural Maintenance of Chromosome Protein 1Ataxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA-Binding Proteinsgamma-H2AX protein, mouseHistonesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesStructural Maintenance of Chromosome Protein 1TelomeraseTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID19071232
PMCPMC2663532
OpenAlexW1997338093

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.