Evidence map›Paper›PMID 23972993›Full record

ArticleCell reports2013

SCF-mediated Cdh1 degradation defines a negative feedback system that coordinates cell-cycle progression.

Hidefumi Fukushima, Kohei Ogura, Lixin Wan, Ying Lu, Victor Li, Daming Gao, Pengda Liu, Alan W Lau, Tao Wu, Marc W Kirschner and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. CDH1 Orchestrates Anabolic Events to Promote Cell Cycle Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Extracellular matrix stiffness regulates degradation of MST2 via SCFBiochimica et biophysica acta. General subjects · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. SCFCell death & disease · 2020
    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

12 authors at 3 institutions in 1 country.

Hidefumi FukushimaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Kohei Ogura
Lixin Wan
Ying Lu
Victor Li
Daming Gao
Pengda Liu
Alan W Lau
Tao Wu
Marc W Kirschner
Hiroyuki Inuzuka
Wenyi Wei
Beth Israel Deaconess Medical Center · USHarvard University · USCenter for Systems Biology · US

Funding

CELL CYCLE REGULATIONR01GM039023 · NIGMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI KIRSCHNER, MARC WALLACE · 1988 to 2017
$10.2M
Interplay between Cdh1 and major regulatory pathways in human cancerR01GM089763 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2009 to 2018
$3.0M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
New insights into the role of the Fbw7 tumor suppressor in senescence and agingK01AG041218 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI INUZUKA, HIROYUKI · 2011 to 2015
$621k
NIA NIH HHS AG041218NIA NIH HHS K01 AG041218NIGMS NIH HHS GM089763NIGMS NIH HHS GM094777NIGMS NIH HHS GM39023NIGMS NIH HHS R01 GM039023NIGMS NIH HHS R01 GM089763NIGMS NIH HHS R01 GM094777
6 · The paper itself

Abstract

Proper cell-cycle transitions are driven by waves of ubiquitin-dependent degradation of key regulators by the anaphase-promoting complex (APC) and Skp1-Cullin1-F-box (SCF) E3 ubiquitin ligase complexes. But precisely how APC and SCF activities are coordinated to regulate cell-cycle progression remains largely unclear. We previously showed that APC/Cdh1 earmarks the SCF component Skp2 for degradation. Here, we continue to report that SCF(β-TRCP) reciprocally controls APC/Cdh1 activity by governing Cdh1 ubiquitination and subsequent degradation. Furthermore, we define both cyclin A and Plk1, two well-known Cdh1 substrates, as upstream modifying enzymes that promote Cdh1 phosphorylation to trigger Cdh1 ubiquitination and subsequent degradation by SCF(β-TRCP). Thus, our work reveals a negative repression mechanism for SCF to control APC, thereby illustrating an elegant dual repression system between these two E3 ligase complexes to create the ordered cascade of APC and SCF activities governing timely cell-cycle transitions.

Indexed as

Cell CycleFeedback, PhysiologicalProteolysisAnaphase-Promoting Complex-CyclosomeAnimalsCdh1 ProteinsCell Cycle ProteinsCyclin AHEK293 CellsHeLa CellsHumansPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsSKP Cullin F-Box Protein LigasesUbiquitinationAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsCell Cycle ProteinsCyclin APolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsSKP Cullin F-Box Protein Ligases

Identifiers

PMID23972993
PMCPMC3839583
OpenAlexW2021375847

What OpenQuestion 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 OpenQuestion graph.