Evidence map›Paper›PMID 26283732›Full record

ArticleMolecular and cellular biology2015

Cdc14A and Cdc14B Redundantly Regulate DNA Double-Strand Break Repair.

Han Lin, Kyungsoo Ha, Guojun Lu, Xiao Fang, Ranran Cheng, Qiuhong Zuo, Pumin Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. SCFCell death & disease · 2020
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

7 authors at 2 institutions in 2 countries.

Han LinDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA.
Kyungsoo HaDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA.
Guojun LuDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA.
Xiao FangDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA.
Ranran ChengBeijing Proteome Research Center, Beijing, China.
Qiuhong ZuoDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA.
Pumin ZhangDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, USA Beijing Proteome Research Center, Beijing, China pzhang@bcm.edu.
Baylor College of Medicine · USBeijing Proteome Research Center · CN

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
Spindle Assembly Checkpoint, Chromosome Stability, and CancerR01CA122623 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ZHANG, PUMIN · 2008 to 2016
$2.8M
The Function of Cdc14B in DNA Damage Repair and TumorigenesisR01CA116097 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ZHANG, PUMIN · 2006 to 2015
$2.6M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS CA116097NCI NIH HHS CA122623NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS R01 CA116097NCI NIH HHS R01 CA122623NCRR NIH HHS S10 RR024574NCRR NIH HHS S10RR024574NIAID NIH HHS P30 AI036211NIAID NIH HHS P30AI036211
6 · The paper itself

Abstract

Cdc14 is a phosphatase that controls mitotic exit and cytokinesis in budding yeast. In mammals, the two Cdc14 homologues, Cdc14A and Cdc14B, have been proposed to regulate DNA damage repair, whereas the mitotic exit and cytokinesis rely on another phosphatase, PP2A-B55α. It is unclear if the two Cdc14s work redundantly in DNA repair and which repair pathways they participate in. More importantly, their target(s) in DNA repair remains elusive. Here we report that Cdc14B knockout (Cdc14B(-/-)) mouse embryonic fibroblasts (MEFs) showed defects in repairing ionizing radiation (IR)-induced DNA double-strand breaks (DSBs), which occurred only at late passages when Cdc14A levels were low. This repair defect could occur at early passages if Cdc14A levels were also compromised. These results indicate redundancy between Cdc14B and Cdc14A in DSB repair. Further, we found that Cdc14B deficiency impaired both homologous recombination (HR) and nonhomologous end joining (NHEJ), the two major DSB repair pathways. We also provide evidence that Cdh1 is a downstream target of Cdc14B in DSB repair.

Indexed as

DNA RepairAnimalsCdh1 ProteinsCell CycleCell LineDNA Breaks, Double-StrandedDNA End-Joining RepairDual-Specificity PhosphatasesFibroblastsGene DeletionMiceMice, Inbred C57BLMice, KnockoutProtein Tyrosine PhosphatasesCDC14A protein, mouseCDC14B protein, mouseCdh1 ProteinsDual-Specificity PhosphatasesFzr1 protein, mouseProtein Tyrosine Phosphatases

Identifiers

PMID26283732
PMCPMC4589603
OpenAlexW2144894650

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.