Evidence map›Paper›PMID 29555767›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

ASK family kinases mediate cellular stress and redox signaling to circadian clock.

Kiyomichi Imamura, Hikari Yoshitane, Kazuki Hattori, Mitsuo Yamaguchi, Kento Yoshida, Takenori Okubo, Isao Naguro, Hidenori Ichijo, Yoshitaka Fukada

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Post-Translational Modifications in Animal Circadian Clocks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  3. Review
  4. Article
  5. Phosphorylation of DNA-binding domains of CLOCK-BMAL1 complex for PER-dependent inhibition in circadian clock of mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Mood phenotypes in rodent models with circadian disturbances.Neurobiology of sleep and circadian rhythms · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Mutation of a PER2 phosphodegron perturbs the circadian phosphoswitch.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Review
  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 1 institution in 1 country.

Kiyomichi ImamuraDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan.
Hikari YoshitaneDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan stane@mail.ecc.u-tokyo.ac.jp sfukada@mail.ecc.u-tokyo.ac.jp.
Kazuki HattoriLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Mitsuo YamaguchiDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan.
Kento YoshidaDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan.
Takenori OkuboDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan.
Isao NaguroLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Hidenori IchijoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Yoshitaka FukadaDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo 113-0033, Japan stane@mail.ecc.u-tokyo.ac.jp sfukada@mail.ecc.u-tokyo.ac.jp.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Daily rhythms of behaviors and physiologies are generated by the circadian clock, which is composed of clock genes and the encoded proteins forming transcriptional/translational feedback loops (TTFLs). The circadian clock is a self-sustained oscillator and flexibly responds to various time cues to synchronize with environmental 24-h cycles. However, the key molecule that transmits cellular stress to the circadian clockwork is unknown. Here we identified apoptosis signal-regulating kinase (ASK), a member of the MAPKKK family, as an essential mediator determining the circadian period and phase of cultured cells in response to osmotic changes of the medium. The physiological impact of ASK signaling was demonstrated by a response of the clock to changes in intracellular redox states. Intriguingly, the TTFLs drive rhythmic expression of

Indexed as

Osmotic PressureAnimalsBehavior, AnimalCircadian ClocksMaleMAP Kinase Kinase Kinase 5MAP Kinase Kinase KinasesMiceMice, Inbred C57BLMice, KnockoutOxidation-ReductionPhosphorylationProtein Processing, Post-TranslationalProteomicsSignal TransductionMap3k15 protein, mouseMap3k5 protein, mouseMAP Kinase Kinase Kinase 5MAP kinase kinase kinase 6MAP Kinase Kinase Kinasesapoptosis signal-regulating kinasecellular stresscircadianphosphorylationredox

Identifiers

PMID29555767
PMCPMC5889649
OpenAlexW2790936534

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.