Evidence map›Paper›PMID 38656683›Full record

ReviewHistology and histopathology2024

The diverse functions of DYRK2 in response to cellular stress.

Akira Kawamura, Saishu Yoshida, Kiyotsugu Yoshida

Abstract readReview
PubMed Publisher
In one paragraph

Review in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 91% 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

2 citing papers in PubMed, 0 citations in OpenAlex.

  1. Article
  2. 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

3 authors at 1 institution in 1 country.

Akira KawamuraDepartment of Biochemistry, The Jikei University School of Medicine, Tokyo, Japan.
Saishu YoshidaDepartment of Biochemistry, The Jikei University School of Medicine, Tokyo, Japan.
Kiyotsugu YoshidaDepartment of Biochemistry, The Jikei University School of Medicine, Tokyo, Japan. kyoshida@jikei.ac.jp.
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To maintain microenvironmental and cellular homeostasis, cells respond to multiple stresses by activating characteristic cellular mechanisms consisting of receptors, signal transducers, and effectors. Dysfunction of these mechanisms can trigger multiple human diseases as well as cancers. Dual-specificity tyrosine-regulated kinases (DYRKs) are members of the CMGC group and are evolutionarily conserved from yeast to mammals. Previous studies revealed that DYRK2 has important roles in the regulation of the cell cycle and survival in cancer cells. On the other hand, recent studies show that DYRK2 also exhibits significant functions in multiple cellular stress responses and in maintaining cellular homeostasis. Hence, the further elucidation of mechanisms underlying DYRK2's diverse responses to various stresses helps to promote the advancement of innovative clinical therapies and pharmacological drugs. This review summarizes the molecular mechanisms of DYRK2, particularly focusing on cellular stress responses.

Indexed as

Dyrk KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesStress, PhysiologicalAnimalsCell CycleHumansNeoplasmsSignal TransductionDyrk KinasesProtein Serine-Threonine KinasesProtein-Tyrosine Kinases

Identifiers

PMID38656683
OpenAlexW4395466721

What Socratic 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 Socratic graph.