Evidence map›Paper›PMID 25303119›Full record

ReviewBiochemistry2015

Emerging models for the molecular basis of mammalian circadian timing.

Chelsea L Gustafson, Carrie L Partch

Abstract readReview
In one paragraph

Review in Biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Oligomerization of PER2 as a dynamic mode of regulation of the mammalian circadian clock.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Uncovering the circadian transcriptome ofProceedings. Biological sciences · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. TRITHORAX-dependent arginine methylation of HSP68 mediates circadian repression by PERIOD in the monarch butterfly.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. The role of circadian rhythm in osteoporosis; a review.Frontiers in cell and developmental biology · 2022
    Review
  15. Article
  16. Review
  17. Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Article
  20. Article
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

2 authors at 2 institutions in 1 country.

Chelsea L GustafsonDepartment of Chemistry and Biochemistry, University of California , Santa Cruz, California 95064, United States.
Carrie L Partch
University of California, San Diego · USUniversity of California, Santa Cruz · US

Funding

Exploring the structural basis for 24-hour timekeeping in mammalsR01GM107069 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI PARTCH, CARRIE L · 2013 to 2020
$3.2M
NIGMS NIH HHS R01 GM107069
6 · The paper itself

Abstract

Mammalian circadian timekeeping arises from a transcription-based feedback loop driven by a set of dedicated clock proteins. At its core, the heterodimeric transcription factor CLOCK:BMAL1 activates expression of Period, Cryptochrome, and Rev-Erb genes, which feed back to repress transcription and create oscillations in gene expression that confer circadian timing cues to cellular processes. The formation of different clock protein complexes throughout this transcriptional cycle helps to establish the intrinsic ∼24 h periodicity of the clock; however, current models of circadian timekeeping lack the explanatory power to fully describe this process. Recent studies confirm the presence of at least three distinct regulatory complexes: a transcriptionally active state comprising the CLOCK:BMAL1 heterodimer with its coactivator CBP/p300, an early repressive state containing PER:CRY complexes, and a late repressive state marked by a poised but inactive, DNA-bound CLOCK:BMAL1:CRY1 complex. In this review, we analyze high-resolution structures of core circadian transcriptional regulators and integrate biochemical data to suggest how remodeling of clock protein complexes may be achieved throughout the 24 h cycle. Defining these detailed mechanisms will provide a foundation for understanding the molecular basis of circadian timing and help to establish new platforms for the discovery of therapeutics to manipulate the clock.

Indexed as

Circadian ClocksAmino Acid SequenceAnimalsCircadian Rhythm Signaling Peptides and ProteinsHumansModels, MolecularMolecular Sequence DataProtein ConformationSequence AlignmentTranscriptional ActivationCircadian Rhythm Signaling Peptides and Proteins

Identifiers

PMID25303119
PMCPMC4303291
OpenAlexW2073713086

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.