Evidence map›Paper›PMID 32372973›Full record

ReviewFrontiers in physiology2020

A Systems Biology Approach Identifies Hidden Regulatory Connections Between the Circadian and Cell-Cycle Checkpoints.

Xianlin Zou, Dae Wook Kim, Tetsuya Gotoh, Jingjing Liu, Jae Kyoung Kim, Carla V Finkielstein

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  6. Biological clock regulation by theFrontiers in cell and developmental biology · 2024
    Review
  7. Chronobiology of Parkinson's disease: Past, present and future.The European journal of neuroscience · 2023
    Review
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  10. 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

6 authors at 2 institutions in 2 countries.

Xianlin ZouIntegrated Cellular Responses Laboratory, Department of Biological Sciences, Fralin Life Sciences Institute, Virginia Tech, Blacksburg, VA, United States.
Dae Wook KimDepartment of Mathematical Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Tetsuya GotohIntegrated Cellular Responses Laboratory, Department of Biological Sciences, Fralin Life Sciences Institute, Virginia Tech, Blacksburg, VA, United States.
Jingjing LiuIntegrated Cellular Responses Laboratory, Department of Biological Sciences, Fralin Life Sciences Institute, Virginia Tech, Blacksburg, VA, United States.
Jae Kyoung KimDepartment of Mathematical Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Carla V FinkielsteinIntegrated Cellular Responses Laboratory, Department of Biological Sciences, Fralin Life Sciences Institute, Virginia Tech, Blacksburg, VA, United States.
Virginia Tech · USKorea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circadian rhythms form a self-sustaining, endogenous, time-keeping system that allows organisms to anticipate daily environmental changes. The core of the clock network consists of interlocking transcriptional-translational feedback loops that ensures that metabolic, behavioral, and physiological processes run on a 24 h timescale. The hierarchical nature of the clock manifests itself in multiple points of control on the daily cell division cycle, which relies on synthesis, degradation, and post-translational modification for progression. This relationship is particularly important for understanding the role of clock components in sensing stress conditions and triggering checkpoint signals that stop cell cycle progression. A case in point is the interplay among the circadian factor PERIOD2 (PER2), the tumor suppressor p53, and the oncogenic mouse double minute-2 homolog protein (MDM2), which is the p53's negative regulator. Under unstressed conditions, PER2 and p53 form a stable complex in the cytosol and, along with MDM2, a trimeric complex in the nucleus. Association of PER2 to the C-terminus end of p53 prevents MDM2-mediated ubiquitylation and degradation of p53 as well as p53's transcriptional activation. Remarkably, when not bound to p53, PER2 acts as substrate for the E3-ligase activity of MDM2; thus, PER2 is degraded in a phosphorylation-independent fashion. Unexpectedly, the phase relationship between PER2 and p53 are opposite; however, a systematic modeling approach, inferred from the oscillatory time course data of PER2 and p53, aided in identifying additional regulatory scenarios that explained,

Indexed as

checkpoint signalingcircadian rhythmsclock genesmathematical modelingp53systematic approachtumor suppressor

Identifiers

PMID32372973
PMCPMC7176909
OpenAlexW3016699241

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.