Evidence map›Paper›PMID 24142690›Full record

ArticleThe Journal of biological chemistry2013

Defect of mitotic vimentin phosphorylation causes microophthalmia and cataract via aneuploidy and senescence in lens epithelial cells.

Makoto Matsuyama, Hiroki Tanaka, Akihito Inoko, Hidemasa Goto, Shigenobu Yonemura, Kyoko Kobori, Yuko Hayashi, Eisaku Kondo, Shigeyoshi Itohara, Ichiro Izawa and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Metal Ion Binding of Vimentin Tail Domain Fragments.Chembiochem : a European journal of chemical biology · 2026
    Article
  3. The important interplay between metal ions and the intermediate filament protein vimentin.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Cellular senescence and ophthalmic diseases: narrative review.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Vimentin and cytokeratin: Good alone, bad together.Seminars in cancer biology · 2022
    Review
  12. Review
  13. Article
  14. Roles of vimentin in health and disease.Genes & development · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. From structural resilience to cell specification - Intermediate filaments as regulators of cell fate.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Review
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

11 authors at 4 institutions in 1 country.

Makoto MatsuyamaFrom the Divisions of Biochemistry and.
Hiroki Tanaka
Akihito Inoko
Hidemasa Goto
Shigenobu Yonemura
Kyoko Kobori
Yuko Hayashi
Eisaku Kondo
Shigeyoshi Itohara
Ichiro Izawa
Masaki Inagaki
Aichi Cancer Center · JPNagoya University · JPRIKEN Center for Brain Science · JPRIKEN Center for Computational Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vimentin, a type III intermediate filament (IF) protein, is phosphorylated predominantly in mitosis. The expression of a phosphorylation-compromised vimentin mutant in T24 cultured cells leads to cytokinetic failure, resulting in binucleation (multinucleation). The physiological significance of intermediate filament phosphorylation during mitosis for organogenesis and tissue homeostasis was uncertain. Here, we generated knock-in mice expressing vimentin that have had the serine sites phosphorylated during mitosis substituted by alanine residues. Homozygotic mice (VIM(SA/SA)) presented with microophthalmia and cataracts in the lens, whereas heterozygotic mice (VIM(WT/SA)) were indistinguishable from WT (VIM(WT/WT)) mice. In VIM(SA/SA) mice, lens epithelial cell number was not only reduced but the cells also exhibited chromosomal instability, including binucleation and aneuploidy. Electron microscopy revealed fiber membranes that were disorganized in the lenses of VIM(SA/SA), reminiscent of similar characteristic changes seen in age-related cataracts. Because the mRNA level of the senescence (aging)-related gene was significantly elevated in samples from VIM(SA/SA), the lens phenotype suggests a possible causal relationship between chromosomal instability and premature aging.

Indexed as

AneuploidyCellular SenescenceMitosisAllelesAmino Acid SequenceAmino Acid SubstitutionAnimalsCataractCell NucleusEndophthalmitisEpithelial CellsGene Knock-In TechniquesLens, CrystallineMiceMolecular Sequence DataPhosphorylationVimentinAneuploidyCataractCell DivisionChromosomal InstabilityCytokinesisMitosisPhosphorylationSenescenceVimentin

Identifiers

PMID24142690
PMCPMC3861614
OpenAlexW1997281289

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.