Evidence map›Paper›PMID 36194579›Full record

ArticlePLoS biology2022

Distinct phosphorylation states of mammalian CaMKIIβ control the induction and maintenance of sleep.

Daisuke Tone, Koji L Ode, Qianhui Zhang, Hiroshi Fujishima, Rikuhiro G Yamada, Yoshiki Nagashima, Katsuhiko Matsumoto, Zhiqing Wen, Shota Y Yoshida, Tomoki T Mitani and 12 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The sleep-wake history contributes to rhythmic BMAL1 chromatin binding in the cerebral cortex but not in the liver.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. CaMKIIβ-mediated Phosphorylation Enhances Protein Stability of Spastin to Promote Neurite Outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Calcineurin governs baseline and homeostatic regulations of non-rapid eye movement sleep in mice.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Developing forebrain synapses are uniquely vulnerable to sleep loss.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. 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

22 authors at 3 institutions in 1 country.

Daisuke ToneLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Koji L OdeLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Qianhui ZhangDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hiroshi FujishimaLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Rikuhiro G YamadaLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Yoshiki NagashimaDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Katsuhiko MatsumotoLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Zhiqing WenDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Shota Y YoshidaLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Tomoki T MitaniLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Yuki ArisatoDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Rei-Ichiro OhnoDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Maki Ukai-TadenumaLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Junko Yoshida GarçonLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Mari KanekoLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Chuo-ku, Kobe, Hyogo, Japan.
Shoi ShiLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Hideki UkaiLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Kazunari MiyamichiLaboratory for Comparative Connections, RIKEN Center for Biosystems Dynamics Research, Chuo-ku, Kobe, Hyogo, Japan.
Takashi OkadaDivision of Molecular and Medical Genetics, Center for Gene and Cell Therapy, The Institute of Medical Science, the University of Tokyo, Minato-city, Tokyo, Japan.
Kenta SumiyamaLaboratory for Mouse Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.
Hiroshi KiyonariLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Chuo-ku, Kobe, Hyogo, Japan.
Hiroki R UedaLaboratory for Synthetic Biology, RIKEN Center for Biosystems Dynamics Research, Suita, Osaka, Japan.ORCID 0000-0001-8342-9176
RIKEN Center for Biosystems Dynamics Research · JPThe University of Tokyo · JPThermo Fisher Scientific (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The reduced sleep duration previously observed in Camk2b knockout mice revealed a role for Ca2+/calmodulin-dependent protein kinase II (CaMKII)β as a sleep-promoting kinase. However, the underlying mechanism by which CaMKIIβ supports sleep regulation is largely unknown. Here, we demonstrate that activation or inhibition of CaMKIIβ can increase or decrease sleep duration in mice by almost 2-fold, supporting the role of CaMKIIβ as a core sleep regulator in mammals. Importantly, we show that this sleep regulation depends on the kinase activity of CaMKIIβ. A CaMKIIβ mutant mimicking the constitutive-active (auto)phosphorylation state promotes the transition from awake state to sleep state, while mutants mimicking subsequent multisite (auto)phosphorylation states suppress the transition from sleep state to awake state. These results suggest that the phosphorylation states of CaMKIIβ differently control sleep induction and maintenance processes, leading us to propose a "phosphorylation hypothesis of sleep" for the molecular control of sleep in mammals.

Indexed as

CalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2AnimalsMammalsMiceMice, KnockoutPhosphorylationSleepCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID36194579
PMCPMC9531794
OpenAlexW4301181076

What OpenQuestion holds

Textmetadata
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.