Evidence map›Paper›PMID 29894471›Full record

ArticlePloS one2018

Modeling circadian variability of core-clock and clock-controlled genes in four tissues of the rat.

Panteleimon D Mavroudis, Debra C DuBois, Richard R Almon, William J Jusko

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Alterations inSleep and biological rhythms · 2024
    Article
  5. Review
  6. Circadian rhythms and the HPA axis: A systems view.WIREs mechanisms of disease · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. It's about time: clocks in the developing lung.The Journal of clinical investigation · 2020
    Review
  12. Review
  13. Review
  14. 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

4 authors at 1 institution in 1 country.

Panteleimon D MavroudisDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, United States of America.ORCID 0000-0002-0512-4147
Debra C DuBoisDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, United States of America.
Richard R AlmonDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, United States of America.
William J JuskoDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York at Buffalo, Buffalo, NY, United States of America.
University at Buffalo, State University of New York · US

Funding

Corticosteroid Pharmacokinetics and PharmacodynamicsR37GM024211 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J. · 2005 to 2014
$6.4M
CORTICOSTEROID PHARMACOKINETICS/DYNAMICSR01GM024211 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J. · 1985 to 2018
$4.7M
NIGMS NIH HHS R01 GM024211NIGMS NIH HHS R37 GM024211
6 · The paper itself

Abstract

Circadian clocks, present in almost all cells of the body, are entrained to rhythmic changes in the environment (e.g. light/dark cycles). Genes responsible for this timekeeping are named core-clock genes, which through transcriptional feedback interactions mediated by transcription factor binding to Ebox/RRE/Dbox elements can generate oscillatory activity of their expression. By regulating the transcription of other clock-controlled genes (CCGs) circadian information is transmitted to tissue and organ levels. Recent studies have indicated that there is a considerable variability of clock-controlled gene expression between tissues both with respect to the circadian genes that are regulated and to their phase lags. In this work, a mathematical model was adapted to explore the dynamics of core-clock and clock-controlled genes measured in four tissues of the rat namely liver, muscle, adipose, and lung. The model efficiently described the synchronous rhythmicity of core-clock genes and further predicted that their phases are mainly regulated by Per2 and Cry1 transcriptional delays and Rev-Erba and Cry1 degradation rates. Similarly, after mining databases for potential Ebox/RRE/Dbox elements in the promoter region of clock-controlled genes, the phase variabilities of the same genes between different tissues were described. The analysis suggests that inter-tissue circadian variability of the same clock-controlled genes is an inherent component of homeostatic function and may arise due to different transcription factor activities on Ebox/RRE/Dbox elements.

Indexed as

Transcription, GeneticAdipose TissueAnimalsCircadian ClocksCircadian RhythmCLOCK ProteinsCryptochromesGene Expression RegulationGene Products, revLiverLungMuscle, SkeletalOrgan SpecificityPeriod Circadian ProteinsPhotoperiodRatsCLOCK ProteinsCry1 protein, ratCryptochromesGene Products, revPer2 protein, ratPeriod Circadian Proteins

Identifiers

PMID29894471
PMCPMC5997360
OpenAlexW2807811942

What OpenQuestion holds

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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.