Evidence map›Paper›PMID 25956863›Full record

ReviewDNA repair2015

Yet another job for Dna2: Checkpoint activation.

Paulina H Wanrooij, Peter M Burgers

Abstract readReview
In one paragraph

Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021
    Article
  7. Article
  8. Article
  9. Inhibition of DNA Repair in Cancer Therapy: Toward a Multi-Target Approach.International journal of molecular sciences · 2020
    Review
  10. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  11. Article
  12. Article
  13. Review
  14. Eukaryotic DNA Replication Fork.Annual review of biochemistry · 2017
    Review
  15. Mutant p53 perturbs DNA replication checkpoint control through TopBP1 and Treslin.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Paulina H WanrooijDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA.
Peter M BurgersDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: burgers@biochem.wustl.edu.
Washington University in St. Louis · US

Funding

ENZYMOLOGY OF REPLICATION OF YEAST CHROMOSOMAL DNAR01GM032431 · NIGMS · WASHINGTON UNIVERSITY · PI BURGERS, PETER M · 1985 to 2015
$6.5M
KINASE ACTIVATION IN THE DNA DAMAGE CHECKPOINTSR01GM083970 · NIGMS · WASHINGTON UNIVERSITY · PI BURGERS, PETER M · 2009 to 2016
$2.1M
NIGMS NIH HHS GM032431NIGMS NIH HHS GM083970NIGMS NIH HHS R01 GM032431NIGMS NIH HHS R01 GM083970
6 · The paper itself

Abstract

Mec1 (ATR in humans) is the principal kinase responsible for checkpoint activation in response to replication stress and DNA damage in Saccharomyces cerevisiae. Checkpoint initiation requires stimulation of Mec1 kinase activity by specific activators. The complexity of checkpoint initiation in yeast increases with the complexity of chromosomal states during the different phases of the cell cycle. In G1 phase, the checkpoint clamp 9-1-1 is both necessary and sufficient for full activation of Mec1 kinase whereas in G2/M, robust checkpoint function requires both 9-1-1 and the replisome assembly protein Dpb11 (human TopBP1). A third activator, Dna2, is employed specifically during S phase to stimulate Mec1 kinase and to initiate the replication checkpoint. Dna2 is an essential nuclease-helicase that is required for proper Okazaki fragment maturation, for double-strand break repair, and for protecting stalled replication forks. Remarkably, all three Mec1 activators use an unstructured region of the protein, containing two critically important aromatic residues, in order to activate Mec1. A role for these checkpoint activators in channeling aberrant replication structures into checkpoint complexes is discussed.

Indexed as

DNA RepairGene Expression Regulation, FungalAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell Cycle ProteinsDNADNA Breaks, Double-StrandedDNA, FungalDNA HelicasesDNA ReplicationHumansIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsDNADNA2 protein, S cerevisiaeDNA, FungalDNA HelicasesDPB11 protein, S cerevisiaeIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeOkazaki fragmentsProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsATRDna2Mec1NucleaseReplication checkpoint

Identifiers

PMID25956863
PMCPMC4522331
OpenAlexW2010170179

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.