Evidence map›Paper›PMID 27892797›Full record

ArticleCell cycle (Georgetown, Tex.)2017

NEK8 regulates DNA damage-induced RAD51 foci formation and replication fork protection.

Antonio Abeyta, Maria Castella, Celine Jacquemont, Toshiyasu Taniguchi

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Checking NEKs: Overcoming a Bottleneck in Human Diseases.Molecules (Basel, Switzerland) · 2020
    Review
  15. Article
  16. Evolution-based screening enables genome-wide prioritization and discovery of DNA repair genes.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Article
  18. Article
  19. Review
  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

4 authors at 2 institutions in 1 country.

Antonio Abeytaa Divisions of Human Biology and Public Health Sciences , Fred Hutchinson Cancer Research Center , Seattle , WA , USA.
Maria Castellaa Divisions of Human Biology and Public Health Sciences , Fred Hutchinson Cancer Research Center , Seattle , WA , USA.
Celine Jacquemonta Divisions of Human Biology and Public Health Sciences , Fred Hutchinson Cancer Research Center , Seattle , WA , USA.
Toshiyasu Taniguchia Divisions of Human Biology and Public Health Sciences , Fred Hutchinson Cancer Research Center , Seattle , WA , USA.
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteins essential for homologous recombination play a pivotal role in the repair of DNA double strand breaks, DNA inter-strand crosslinks and replication fork stability. Defects in homologous recombination also play a critical role in the development of cancer and the sensitivity of these cancers to chemotherapy. RAD51, an essential factor for homologous recombination and replication fork protection, accumulates and forms immunocytochemically detectable nuclear foci at sites of DNA damage. To identify kinases that may regulate RAD51 localization to sites of DNA damage, we performed a human kinome siRNA library screen, using DNA damage-induced RAD51 foci formation as readout. We found that NEK8, a NIMA family kinase member, is required for efficient DNA damage-induced RAD51 foci formation. Interestingly, knockout of Nek8 in murine embryonic fibroblasts led to cellular sensitivity to the replication inhibitor, hydroxyurea, and inhibition of the ATR kinase. Furthermore, NEK8 was required for proper replication fork protection following replication stall with hydroxyurea. Loading of RAD51 to chromatin was decreased in NEK8-depleted cells and Nek8-knockout cells. Single-molecule DNA fiber analyses revealed that nascent DNA tracts were degraded in the absence of NEK8 following treatment with hydroxyurea. Consistent with this, Nek8-knockout cells showed increased chromosome breaks following treatment with hydroxyurea. Thus, NEK8 plays a critical role in replication fork stability through its regulation of the DNA repair and replication fork protection protein RAD51.

Indexed as

DNA DamageDNA ReplicationGenomic InstabilityHeLa CellsHomologous RecombinationHumansNIMA-Related KinasesRad51 RecombinaseRNA, Small InterferingStress, PhysiologicalNEK8 protein, humanNek8 protein, mouseNIMA-Related KinasesRad51 RecombinaseRNA, Small InterferingDNA repairgenome instabilityhomologous recombinationNEK8RAD51replication fork protection

Identifiers

PMID27892797
PMCPMC5324754
OpenAlexW2559080730

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.