Evidence map›Paper›PMID 12686604›Full record

ArticleMolecular biology of the cell2003

Functional significance of the specific sites phosphorylated in desmin at cleavage furrow: Aurora-B may phosphorylate and regulate type III intermediate filaments during cytokinesis coordinatedly with Rho-kinase.

Aie Kawajiri, Yoshihiro Yasui, Hidemasa Goto, Masaaki Tatsuka, Masahide Takahashi, Koh-Ichi Nagata, Masaki Inagaki

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-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

39 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Alexander disease: models, mechanisms, and medicine.Current opinion in neurobiology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Intermediate filaments and IF-associated proteins: from cell architecture to cell proliferation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Myofibril breakdown during atrophy is a delayed response requiring the transcription factor PAX4 and desmin depolymerization.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. The Aurora kinase inhibitors in cancer research and therapy.Journal of cancer research and clinical oncology · 2016
    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

7 authors at 3 institutions in 1 country.

Aie KawajiriDivision of Biochemistry, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464-8681, Japan.
Yoshihiro Yasui
Hidemasa Goto
Masaaki Tatsuka
Masahide Takahashi
Koh-Ichi Nagata
Masaki Inagaki
Aichi Cancer Center · JPNagoya University · JPHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora-B is a protein kinase required for chromosome segregation and the progression of cytokinesis during the cell cycle. We report here that Aurora-B phosphorylates GFAP and desmin in vitro, and this phosphorylation leads to a reduction in filament forming ability. The sites phosphorylated by Aurora-B; Thr-7/Ser-13/Ser-38 of GFAP, and Thr-16 of desmin are common with those related to Rho-associated kinase (Rho-kinase), which has been reported to phosphorylate GFAP and desmin at cleavage furrow during cytokinesis. We identified Ser-59 of desmin to be a specific site phosphorylated by Aurora-B in vitro. Use of an antibody that specifically recognized desmin phosphorylated at Ser-59 led to the finding that the site is also phosphorylated specifically at the cleavage furrow during cytokinesis in Saos-2 cells. Desmin mutants, in which in vitro phosphorylation sites by Aurora-B and/or Rho-kinase are changed to Ala or Gly, cause dramatic defects in filament separation between daughter cells in cytokinesis. The results presented here suggest the possibility that Aurora-B may regulate cleavage furrow-specific phosphorylation and segregation of type III IFs coordinatedly with Rho-kinase during cytokinesis.

Indexed as

Amino Acid SequenceAnimalsAurora Kinase BAurora KinasesBinding SitesCell DivisionCell LineCOS CellsDesminGlial Fibrillary Acidic ProteinHumansIntermediate FilamentsIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesMolecular Sequence DataMutagenesis, Site-DirectedAURKB protein, humanAurora Kinase BAurora KinasesDesminGlial Fibrillary Acidic ProteinIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesRecombinant Fusion Proteinsrho-Associated KinasesSerine

Identifiers

PMID12686604
PMCPMC153117
OpenAlexW2166470703

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.