Evidence map›Paper›PMID 12381662›Full record

ArticleGenes & development2002

Disruption of mCry2 restores circadian rhythmicity in mPer2 mutant mice.

Henrik Oster, Akira Yasui, Gijsbertus T J van der Horst, Urs Albrecht

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
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  6. Decanalizing thinking on genetic canalization.Seminars in cell & developmental biology · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Early doors (Edo) mutant mouse reveals the importance of period 2 (PER2) PAS domain structure for circadian pacemaking.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Article
  12. Review
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  16. Dual roles of FBXL3 in the mammalian circadian feedback loops are important for period determination and robustness of the clock.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
  18. Review
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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

4 authors at 3 institutions in 4 countries.

Henrik OsterMax Planck Institute for Experimental Endocrinology, 30625 Hannover, Germany.
Akira Yasui
Gijsbertus T J van der Horst
Urs Albrecht
Erasmus University Rotterdam · NLMax Planck Institute for Biophysical Chemistry · DETohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many biochemical, physiological, and behavioral processes display daily rhythms generated by an internal timekeeping mechanism referred to as the circadian clock. The core oscillator driving this clock is located in the ventral part of the hypothalamus, the so called suprachiasmatic nuclei (SCN). At the molecular level, this oscillator is thought to be composed of interlocking autoregulatory feedback loops involving a set of clock genes. Among the components driving the mammalian circadian clock are the Period 1 and 2 (mPer1 and mPer2) and Cryptochrome 1 and 2 (mCry1 and mCry2) genes. A mutation in the mPer2 gene leads to a gradual loss of circadian rhythmicity in mice kept in constant darkness (DD). Here we show that inactivation of the mCry2 gene in mPer2 mutant mice restores circadian rhythmicity and normal clock gene expression patterns. Thus, mCry2 can act as a nonallelic suppressor of mPer2, which points to direct or indirect interactions of PER2 and CRY2 proteins. In marked contrast, inactivation of mCry1 in mPer2 mutant mice does not restore circadian rhythmicity but instead results in complete behavioral arrhythmicity in DD, indicating different effects of mCry1 and mCry2 in the clock mechanism

Indexed as

Drosophila ProteinsEye ProteinsPhotoreceptor Cells, InvertebrateAnimalsBiological ClocksBlotting, NorthernCell Cycle ProteinsCircadian RhythmCryptochromesFlavoproteinsGene Expression RegulationGenes, DominantIn Situ HybridizationKidneyMiceMice, KnockoutCell Cycle ProteinsCry2 protein, mousecry protein, DrosophilaCryptochromesDrosophila ProteinsEye ProteinsFlavoproteinsNuclear ProteinsPer2 protein, mousePeriod Circadian ProteinsReceptors, G-Protein-CoupledRNA, MessengerTranscription Factors

Identifiers

PMID12381662
PMCPMC187457
OpenAlexW2041920429

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.