Evidence map›Paper›PMID 30290241›Full record

ReviewBiochimica et biophysica acta. Molecular cell research2018

Who guards the guardian? Mechanisms that restrain APC/C during the cell cycle.

Jennifer Kernan, Thomas Bonacci, Michael J Emanuele

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.2field-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

36 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Cellular senescence as a source of chronic microinflammation that promotes the aging process.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. CDK4/6 inhibitors downregulate the ubiquitin-conjugating enzymes UBE2C/S/T involved in the ubiquitin-proteasome pathway in ER + breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  10. Article
  11. Article
  12. Examining the mechanistic relationship of APC/CProtein science : a publication of the Protein Society · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Identification ofOncology letters · 2021
    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

3 authors at 1 institution in 1 country.

Jennifer KernanLineberger Comprehensive Cancer Center, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States of America.
Thomas BonacciLineberger Comprehensive Cancer Center, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States of America.
Michael J EmanueleLineberger Comprehensive Cancer Center, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States of America. Electronic address: emanuele@email.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

SCF Ubiquitin Ligases in Cell Cycle Control and Chromosome StabilityR01GM120309 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI EMANUELE, MICHAEL JAMES · 2016 to 2023
$2.3M
NIGMS NIH HHS R01 GM120309
6 · The paper itself

Abstract

The cell cycle is principally controlled by Cyclin Dependent Kinases (CDKs), whose oscillating activities are determined by binding to Cyclin coactivators. Cyclins exhibit dynamic changes in abundance as cells pass through the cell cycle. The sequential, timed accumulation and degradation of Cyclins, as well as many other proteins, imposes order on the cell cycle and contributes to genome maintenance. The destruction of many cell cycle regulated proteins, including Cyclins A and B, is controlled by a large, multi-subunit E3 ubiquitin ligase termed the Anaphase Promoting Complex/Cyclosome (APC/C). APC/C activity is tightly regulated during the cell cycle. Its activation state increases dramatically in mid-mitosis and it remains active until the end of G1 phase. Following its mandatory inactivation at the G1/S boundary, APC/C activity remains low until the subsequent mitosis. Due to its role in guarding against the inappropriate or untimely accumulation of Cyclins, the APC/C is a core component of the cell cycle oscillator. In addition to the regulation of Cyclins, APC/C controls the degradation of many other substrates. Therefore, it is vital that the activity of APC/C itself be tightly guarded. The APC/C is most well studied for its role and regulation during mitosis. However, the APC/C also plays a similarly important and conserved role in the maintenance of G1 phase. Here we review the diverse mechanisms counteracting APC/C activity throughout the cell cycle and the importance of their coordinated actions on cell growth, proliferation, and disease.

Indexed as

Anaphase-Promoting Complex-CyclosomeAnimalsCell CycleCell ProliferationCyclin-Dependent KinasesCyclinsGene Expression RegulationHumansAnaphase-Promoting Complex-CyclosomeCyclin-Dependent KinasesCyclinsAPC/CCell cycleDeubiquitinating enzyme (DUB)ProteolysisUbiquitinUbiquitin ligase

Identifiers

PMID30290241
PMCPMC6198803
OpenAlexW2895543470

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.