Evidence map›Paper›PMID 30516086›Full record

ArticleCell cycle (Georgetown, Tex.)2018

Destabilization of the MiniChromosome Maintenance (MCM) complex modulates the cellular response to DNA double strand breaks.

Romain Drissi, Anaïs Chauvin, Alyson McKenna, Dominique Lévesque, Simon Blais-Brochu, Dominique Jean, François-Michel Boisvert

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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 1 institution in 1 country.

Romain Drissia Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.
Anaïs Chauvina Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.ORCID 0000-0002-2430-2316
Alyson McKennaa Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.
Dominique Lévesquea Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.
Simon Blais-Brochua Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.
Dominique Jeana Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.ORCID 0000-0003-4546-9796
François-Michel Boisverta Department of Anatomy and Cell Biology , Université de Sherbrooke , 3201 Jean-Mignaul, Sherbrooke , Québec , Canada.ORCID 0000-0001-8882-8619
Université de Sherbrooke · CA

Funding

CIHR MOP-123469
6 · The paper itself

Abstract

DNA replication during S phase involves thousands of replication forks that must be coordinated to ensure that every DNA section is replicated only once. The minichromosome maintenance proteins, MCM2 to MCM7, form a heteromeric DNA helicase required for both the initiation and elongation of DNA replication. Although only two DNA helicase activities are necessary to establish a bidirectional replication fork from each replication origin, a large excess of MCM complexes is amassed and distributed along the chromatin. The function of the additional MCM complexes is not well understood, as most are displaced from the DNA during the S-phase, apparently without playing an active role in DNA replication. DNA damage response (DDR) kinases activated by stalled forks prevent the replication machinery from being activated, indicating a tight relationship between DDR and DNA replication. To investigate the role of MCM proteins in the cellular response to DNA damage, we used shRNA targeting MCM2 or MCM3 to determine the impact of a reduction in MCM complex. The alteration of MCM proteins induced a change in the activation of key factors of the DDR in response to Etoposide treatment. Etoposide-induced DNA damage affected the phosphorylation of γ-H2AX, CHK1 and CHK2 without affecting cell viability. Using assays measuring homologous recombination (HR) and non-homologous end-joining (NHEJ), we identified a decrease in both HR and NHEJ associated with a decrease in MCM complex.

Indexed as

DNA Breaks, Double-StrandedCell Line, TumorChromatography, High Pressure LiquidDNA End-Joining RepairEtoposideG1 Phase Cell Cycle CheckpointsHistonesHomologous RecombinationHumansMass SpectrometryMinichromosome Maintenance Complex Component 2Minichromosome Maintenance Complex Component 3Minichromosome Maintenance ProteinsPhosphopeptidesPhosphorylationRNA InterferenceEtoposideH2AX protein, humanHistonesMCM2 protein, humanMCM3 protein, humanMinichromosome Maintenance Complex Component 2Minichromosome Maintenance Complex Component 3Minichromosome Maintenance ProteinsPhosphopeptidesRNA, Small InterferingDNA damageDNA repairEtoposideHomologous RecombinationMCM protein

Identifiers

PMID30516086
PMCPMC6300108
OpenAlexW2905043436

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.