Evidence map›Paper›PMID 26617050›Full record

ArticleNature communications2015

A tunable artificial circadian clock in clock-defective mice.

Matthew D'Alessandro, Stephen Beesley, Jae Kyoung Kim, Rongmin Chen, Estela Abich, Wayne Cheng, Paul Yi, Joseph S Takahashi, Choogon Lee

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. PERspectives on circadian cell biology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  4. Review
  5. Review
  6. Article
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  9. Coupling-dependent metabolic ultradian rhythms in confluent cells.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  11. Article
  12. Review
  13. Article
  14. Wake-sleep cycles are severely disrupted by diseases affecting cytoplasmic homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
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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

9 authors at 3 institutions in 2 countries.

Matthew D'AlessandroDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Stephen BeesleyDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Jae Kyoung KimMathematical Biosciences Institute, The Ohio State University, 1735 Neil Avenue, Columbus, Ohio 43210, USA.
Rongmin ChenDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Estela AbichDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Wayne ChengDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Paul YiDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Joseph S TakahashiHoward Hughes Medical Institute, Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Choogon LeeDepartment of Biomedical Sciences, Program in Neuroscience, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306, USA.
Florida State University · USKorea Advanced Institute of Science and Technology · KRThe University of Texas Southwestern Medical Center · US

Funding

NO Dysregulation of the Peripheral Clock in Diabetic ComplicationsR01DK090730 · NIDDK · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO · 2010 to 2013
$1.3M
NIDDK NIH HHS DK-090730NIDDK NIH HHS R01 DK090730
6 · The paper itself

Abstract

Self-sustaining oscillations are essential for diverse physiological functions such as the cell cycle, insulin secretion and circadian rhythms. Synthetic oscillators using biochemical feedback circuits have been generated in cell culture. These synthetic systems provide important insight into design principles for biological oscillators, but have limited similarity to physiological pathways. Here we report the generation of an artificial, mammalian circadian clock in vivo, capable of generating robust, tunable circadian rhythms. In mice deficient in Per1 and Per2 genes (thus lacking circadian rhythms), we artificially generate PER2 rhythms and restore circadian sleep/wake cycles with an inducible Per2 transgene. Our artificial clock is tunable as the period and phase of the rhythms can be modulated predictably. This feature, and other design principles of our work, might enhance the study and treatment of circadian dysfunction and broader aspects of physiology involving biological oscillators.

Indexed as

Circadian ClocksAnimalsChronobiology DisordersDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutPeriod Circadian ProteinsPer1 protein, mousePer2 protein, mousePeriod Circadian Proteins

Identifiers

PMID26617050
PMCPMC4674671
OpenAlexW2186462130

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.