Evidence map›Paper›PMID 24481920›Full record

ArticleChromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology2014

The CENP-O complex requirement varies among different cell types.

Naoko Kagawa, Tetsuya Hori, Yuko Hoki, Osamu Hosoya, Kimiko Tsutsui, Yumiko Saga, Takashi Sado, Tatsuo Fukagawa

Open access · hybridAbstract read
In one paragraph

Article in Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Molecular evolution of the mammalian kinetochore complex.bioRxiv : the preprint server for biology · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Kinetochore Architecture Employs Diverse Linker Strategies Across Evolution.Frontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. Mitosis-related geneAnnals of translational medicine · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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 4 institutions in 1 country.

Naoko KagawaDepartment of Molecular Genetics, National Institute of Genetics and The Graduate University for Advanced Studies, Mishima, Shizuoka, 411-8540, Japan.
Tetsuya Hori
Yuko Hoki
Osamu Hosoya
Kimiko Tsutsui
Yumiko Saga
Takashi Sado
Tatsuo Fukagawa
Kyushu University · JPNational Institute of Genetics · JPOkayama University · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CENP-U (CENP-50) is a component of the CENP-O complex, which includes CENP-O, CENP-P, CENP-Q, CENP-R, and CENP-U and is constitutively localized at kinetochores throughout the cell cycle in vertebrates. Although CENP-U deficiency results in some mitotic defects in chicken DT40 cells, CENP-U-deficient chicken DT40 cells are viable. To examine the functional roles of CENP-U in an organism-dependent context, we generated CENP-U-deficient mice. The CENP-U-deficient mice died during early embryogenesis (approximately E7.5). Thus, conditional CENP-U-deficient mouse ES cells were generated to analyze CENP-U-deficient phenotypes at the cell level. When CENP-U was disrupted in the mouse ES cells, all CENP-O complex proteins disappeared from kinetochores. In contrast, other kinetochore proteins were recruited in CENP-U-deficient mouse ES cells as CENP-U-deficient DT40 cells. However, the CENP-U-deficient ES cells died after exhibiting abnormal mitotic behavior. Although CENP-U was essential for cell viability during mouse early embryogenesis, CENP-U-deficient mouse embryonic fibroblast cells were viable, similar to the DT40 cells. Thus, although both DT40 and ES cells with CENP-U deficiency have similar mitotic defects, cellular responses to mitotic defects vary among different cell types.

Indexed as

Organ SpecificityAnimalsCell LineCell SurvivalChickensChromosomal Proteins, Non-HistoneChromosome AberrationsEmbryonic DevelopmentEmbryonic Stem CellsFibroblastsMiceMitosisMultiprotein ComplexesProtein TransportChromosomal Proteins, Non-HistoneMultiprotein Complexes

Identifiers

PMID24481920
PMCPMC4129241
OpenAlexW2006730485

What OpenQuestion holds

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LicenceCC BY
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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.