Evidence map›Paper›PMID 26530630›Full record

ArticleScientific reports2015

Lats1 suppresses centrosome overduplication by modulating the stability of Cdc25B.

Satomi Mukai, Norikazu Yabuta, Kaori Yoshida, Ayumi Okamoto, Daisaku Miura, Yasuhide Furuta, Takaya Abe, Hiroshi Nojima

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. TheCells · 2021
    Review
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  13. Article
  14. Article
  15. Review
  16. Article
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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

8 authors at 3 institutions in 1 country.

Satomi MukaiDepartment of Molecular Genetics Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita City, Osaka 565-0871, Japan.
Norikazu YabutaDepartment of Molecular Genetics Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita City, Osaka 565-0871, Japan.
Kaori YoshidaDepartment of Molecular Genetics Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita City, Osaka 565-0871, Japan.
Ayumi OkamotoDepartment of Molecular Genetics Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita City, Osaka 565-0871, Japan.
Daisaku MiuraDepartment of Pharmacy, Hyogo University of Health Sciences, Kobe, Japan.
Yasuhide FurutaAnimal Resource Development Unit, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Takaya AbeAnimal Resource Development Unit, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Hiroshi NojimaDepartment of Molecular Genetics Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita City, Osaka 565-0871, Japan.
Osaka University · JPGenetic Resources Center · JPHyogo University of Health Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerical aberration of the centrosome results in chromosome missegregation, eventually leading to chromosomal instability, a hallmark of human tumor malignancy. Large tumor suppressors 1 and 2 (Lats1 and Lats2) are central kinases in the Hippo pathway and regulate development and tumorigenesis by coordinating the balance between cell proliferation and apoptosis. Importantly, Lats1 and Lats2 also play pivotal roles in cell cycle checkpoint and mitosis. The Lats proteins localize at centrosomes, but their centrosomal functions remain elusive. Here, we generated Lats1-null knockout (Lats1(-/-)) mice and established Lats1-null mouse embryonic fibroblasts (MEFs). In Lats1(-/-) MEFs, centrosomes were markedly overduplicated, leading to severe mitotic defects such as chromosome missegregation and cytokinesis failure. We also found that Lats1 physically interacts with Cdc25B phosphatase that localizes both at the centrosome and in the nucleus and regulates the linkage between the centrosome cycle and mitotic progression. Although Lats1 did not phosphorylate Cdc25B, loss of Lats1 in MEFs caused abnormal accumulation of Cdc25B protein and hyperactivation of Cdk2 toward nucleophosmin (NPM/B23), one of the licensing factors involved in centriole duplication. Taken together, these data suggest that Lats1 regulates Cdc25B protein level and subsequent Cdk2 activity, thereby suppressing centrosome overduplication during interphase.

Indexed as

Animalscdc25 PhosphatasesCell DivisionCell LineCentrosomeCyclin-Dependent Kinase 2CytokinesisG2 PhaseHEK293 CellsHumansMiceMice, KnockoutMicroscopy, FluorescenceMitosisNuclear ProteinsNucleophosminCdc25b protein, mousecdc25 PhosphatasesCyclin-Dependent Kinase 2Lats1 protein, mouseNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosminProtein Serine-Threonine KinasesRNA, Small Interfering

Identifiers

PMID26530630
PMCPMC4632022
OpenAlexW2411935113

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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.