Evidence map›Paper›PMID 25603354›Full record

ReviewCell cycle (Georgetown, Tex.)2015

Engagement of DYRK2 in proper control for cell division.

Naoe Taira Nihira, Kiyotsugu Yoshida

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  5. Article
  6. Functional Roles of DYRK2 as a Tumor Regulator.Current issues in molecular biology · 2023
    Review
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  17. Review
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  19. Article
  20. Tuning the proteasome to brighten the end of the journey.American journal of physiology. Cell physiology · 2016
    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

2 authors at 1 institution in 1 country.

Naoe Taira Nihiraa Department of Biochemistry ; The Jikei University School of Medicine ; Minato-ku , Tokyo , Japan.
Kiyotsugu Yoshida
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of cell cycle machinery causes abnormal cell division, leading to cancer development. To drive cell cycle properly, expression levels of cell cycle regulators are tightly regulated through the cell cycle. Dual specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) is a Ser/Thr kinase, and its intracellular functions had not been elucidated for decades. Recent studies have shown that DYRK2 down-regulates key molecules on cell cycle control. This review mainly highlights the DYRK2 function during cell division. In addition, we summarize tumor suppressive role of DYRK2 in cancer cells and discuss future research directions for DYRK2 toward the novel cancer therapies.

Indexed as

Cell DivisionAnimalsDyrk KinasesHumansModels, BiologicalMutationNeoplasmsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesUbiquitin-Protein LigasesDyrk KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesUbiquitin-Protein Ligasesapoptosiscell cycle regulationDYRK2EMTproteasomal degradation

Identifiers

PMID25603354
PMCPMC4613861
OpenAlexW1487848166

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.