Evidence map›Paper›PMID 25271155›Full record

ArticleThe Journal of biological chemistry2014

The mammalian circadian clock protein period counteracts cryptochrome in phosphorylation dynamics of circadian locomotor output cycles kaput (CLOCK).

Ritsuko Matsumura, Yoshiki Tsuchiya, Isao Tokuda, Takahiro Matsuo, Miho Sato, Koichi Node, Eisuke Nishida, Makoto Akashi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. The CLOCK-BMAL1 complex in circadian regulation: structure, mechanisms, and therapeutic targeting.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. The Molecular Mechanism ofInternational journal of molecular sciences · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Inhibition of Expression of the Circadian Clock GeneInternational journal of molecular sciences · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Introduction to the Clock System.Advances in experimental medicine and biology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

8 authors at 4 institutions in 1 country.

Ritsuko MatsumuraResearch Institute for Time Studies, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8511, Japan.
Yoshiki TsuchiyaDepartment of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
Isao TokudaDepartment of Mechanical Engineering, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu 525-8577, Japan, and.
Takahiro MatsuoResearch Institute for Time Studies, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8511, Japan.
Miho SatoResearch Institute for Time Studies, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8511, Japan.
Koichi NodeDepartment of Cardiovascular Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan.
Eisuke NishidaDepartment of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
Makoto AkashiResearch Institute for Time Studies, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8511, Japan,. Electronic address: akashima@yamaguchi-u.ac.jp.
Yamaguchi University · JPKyoto University · JPRitsumeikan University · JPSaga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The circadian transcription factor CLOCK exhibits a circadian oscillation in its phosphorylation levels. Although it remains unclear whether this phosphorylation contributes to circadian rhythm generation, it has been suggested to be involved in transcriptional activity, intracellular localization, and degradative turnover of CLOCK. Here, we obtained direct evidence that CLOCK phosphorylation may be essential for autonomous circadian oscillation in clock gene expression. Importantly, we found that the circadian transcriptional repressors Cryptochrome (CRY) and Period (PER) showed an opposite effect on CLOCK phosphorylation; CRY impaired BMAL1-dependent CLOCK phosphorylation, whereas PER protected the phosphorylation against CRY. Interestingly, unlike PER1 and PER2, PER3 did not exert a protective action, which correlates with the phenotypic differences among mice lacking the Per genes. Further studies on the regulatory mechanism of CLOCK phosphorylation would thus lead to elucidation of the mechanism of CRY-mediated transcriptional repression and an understanding of the true role of PER in the negative feedback system.

Indexed as

AnimalsARNTL Transcription FactorsBrainCell NucleusCLOCK ProteinsCryptochromesMiceMice, TransgenicModels, TheoreticalNIH 3T3 CellsOscillometryPeriod Circadian ProteinsPhosphorylationPromoter Regions, GeneticSuprachiasmatic NucleusARNTL Transcription FactorsBmal1 protein, mouseClock protein, mouseCLOCK ProteinsCryptochromesPer1 protein, mousePer2 protein, mousePer3 protein, mousePeriod Circadian ProteinsCircadian ClockCircadian RhythmClock GeneGene ExpressionPhosphorylation

Identifiers

PMID25271155
PMCPMC4231683
OpenAlexW2082668109

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.