Evidence map›Paper›PMID 26460953›Full record

ArticleOncotarget2015

PRMT1 promotes mitosis of cancer cells through arginine methylation of INCENP.

Xiaolan Deng, Gottfried Von Keudell, Takehiro Suzuki, Naoshi Dohmae, Makoto Nakakido, Lianhua Piao, Yuichiro Yoshioka, Yusuke Nakamura, Ryuji Hamamoto

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. [PRMT1 inhibits apoptosis of nasopharyngeal carcinoma cells by promoting RRM2 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  12. Review
  13. Structure, Activity, and Function of PRMT1.Life (Basel, Switzerland) · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  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

9 authors at 3 institutions in 3 countries.

Xiaolan DengSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Gottfried Von KeudellSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Takehiro SuzukiBiomolecular Characterization Unit, RIKEN Center for Sustainable Resource Science, Wako, Saitama, Japan.
Naoshi DohmaeBiomolecular Characterization Unit, RIKEN Center for Sustainable Resource Science, Wako, Saitama, Japan.
Makoto NakakidoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Lianhua PiaoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Yuichiro YoshiokaSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Yusuke NakamuraSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
Ryuji HamamotoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL, USA.
University of Chicago · USRIKEN Center for Sustainable Resource Science · JPChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inner centromere protein (INCENP) is a part of a protein complex known as the chromosomal passenger complex (CPC) that is essential for correcting non-bipolar chromosome attachments and for cytokinesis. We here demonstrate that a protein arginine methyltransferase PRMT1, which are overexpressed in various types of cancer including lung and bladder cancer, methylates arginine 887 in an Aurora Kinase B (AURKB)-binding region of INCENP both in vitro and in vivo. R887-substituted INCENP revealed lower binding-affinity to AURKB than wild-type INCENP in the presence of PRMT1. Knockdown of PRMT1 as well as overexpression of methylation-inactive INCENP attenuated the AURKB activity in cancer cells, and resulted in abnormal chromosomal alignment and segregation. Furthermore, introduction of methylation-inactive INCENP into cancer cells reduced the growth rate, compared with those introduced wild-type INCENP or Mock. Our data unveils a novel mechanism of PRMT1-mediated CPC regulation through methylation of INCENP.

Indexed as

Amino Acid SequenceArginineCell Line, TumorChromosomal Proteins, Non-HistoneHEK293 CellsHeLa CellsHumansMethylationMitosisMolecular Sequence DataNeoplasmsProtein-Arginine N-MethyltransferasesRepressor ProteinsTransfectionArginineChromosomal Proteins, Non-HistoneINCENP protein, humanPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRepressor Proteinsarginine methylationAurora kinase BINCENPPRMT1

Identifiers

PMID26460953
PMCPMC4742097
OpenAlexW2173265159

What OpenQuestion holds

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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.