Evidence map›Paper›PMID 19015239›Full record

ArticleMolecular and cellular biology2009

Artemis and nonhomologous end joining-independent influence of DNA-dependent protein kinase catalytic subunit on chromosome stability.

Travis H Stracker, Bret R Williams, Ludovic Deriano, Jan W Theunissen, Carrie A Adelman, David B Roth, John H J Petrini

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The MRE11 complex: starting from the ends.Nature reviews. Molecular cell biology · 2011
    Review
  8. Article
  9. Article
  10. Article
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 4 institutions in 1 country.

Travis H StrackerMolecular Biology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center and Cornell University Graduate School of Medical Sciences, New York, NY 10065, USA.
Bret R Williams
Ludovic Deriano
Jan W Theunissen
Carrie A Adelman
David B Roth
John H J Petrini
Cornell University · USMemorial Sloan Kettering Cancer Center · USNew York University · USUniversity of Wisconsin–Madison · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
ROLES OF MRELL AND RAD50 IN THE DNA DAMAGE RESPONSER01GM056888 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1998 to 2019
$8.6M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
FASEB SRC on Genetic Recombination and Genome RearrangementsR13CA162528 · NCI · FEDERATION OF AMER SOC FOR EXPER BIOLOGY · PI PETRINI, JOHN HJ · 2011 to 2011
$5k
NCI NIH HHS P30 CA008748NCI NIH HHS R13 CA162528NIGMS NIH HHS R01 GM056888NIGMS NIH HHS R01 GM059413
6 · The paper itself

Abstract

Deficiency in both ATM and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is synthetically lethal in developing mouse embryos. Using mice that phenocopy diverse aspects of Atm deficiency, we have analyzed the genetic requirements for embryonic lethality in the absence of functional DNA-PKcs. Similar to the loss of ATM, hypomorphic mutations of Mre11 (Mre11(ATLD1)) led to synthetic lethality when juxtaposed with DNA-PKcs deficiency (Prkdc(scid)). In contrast, the more moderate DNA double-strand break response defects associated with the Nbs1(DeltaB) allele permitted viability of some Nbs1(DeltaB/DeltaB) Prkdc(scid/scid) embryos. Cell cultures from Nbs1(DeltaB/DeltaB) Prkdc(scid/scid) embryos displayed severe defects, including premature senescence, mitotic aberrations, sensitivity to ionizing radiation, altered checkpoint responses, and increased chromosome instability. The known functions of DNA-PKcs in the regulation of Artemis nuclease activity or nonhomologous end joining-mediated repair do not appear to underlie the severe genetic interaction. Our results reveal a role for DNA-PKcs in the maintenance of S/G(2)-phase chromosome stability and in the induction of cell cycle checkpoint responses.

Indexed as

Chromosomal InstabilityAnimalsAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCell DeathChromosomal Proteins, Non-HistoneDNA-Activated Protein KinaseDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairDNA Repair EnzymesEmbryo, MammalianEndonucleasesG2 PhaseMiceAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsChromosomal Proteins, Non-HistoneDclre1c protein, mouseDNA-Activated Protein KinaseDNA-Binding ProteinsDNA Repair EnzymesEndonucleasesMre11a protein, mouseMRE11 Homologue ProteinNijmegen breakage syndrome 1 protein, mouseNuclear ProteinsPrkdc protein, mouseProtein Serine-Threonine KinasesStructural Maintenance of Chromosome Protein 1Tumor Suppressor Proteins

Identifiers

PMID19015239
PMCPMC2612508
OpenAlexW2117240918

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.