Evidence map›Paper›PMID 21403396›Full record

ArticleThe Journal of clinical investigation2011

Good COP1 or bad COP1? In vivo veritas.

Wenyi Wei, William G Kaelin

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. EGF Relays Signals to COP1 and Facilitates FOXO4 Degradation to Promote Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    Article
  3. Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. High expression of constitutive photomorphogenic 1 (COP1) is associated with poor prognosis in bladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
William G Kaelin
Beth Israel Deaconess Medical Center · USHoward Hughes Medical Institute · US

Funding

Treating the P13-Kinase/AKTP50CA101942 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Wanling Xie · 2003 to 2026
$53.4M
The von Hippel-Lindau Tumor Suppressor Protein:Roles in Cancer and Oxygen SensingR01CA068490 · NCI · DANA-FARBER CANCER INSTITUTE · PI KAELIN, WILLIAM G. · 1996 to 2015
$4.8M
Interplay between Cdh1 and major regulatory pathways in human cancerR01GM089763 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2009 to 2018
$3.0M
Howard Hughes Medical InstituteNCI NIH HHS CA068490NCI NIH HHS CA101942NCI NIH HHS P50 CA101942NCI NIH HHS R01 CA068490NIGMS NIH HHS GM089763NIGMS NIH HHS R01 GM089763
6 · The paper itself

Abstract

The evolutionarily conserved protein COP1 has been shown to operate as an E3 ubiquitin ligase complex, and a number of putative substrates have been identified, including the c-JUN oncoprotein and p53 tumor suppressor protein. New work by Migliorini and colleagues described in the current issue of JCI demonstrates that COP1 acts as a tumor suppressor in vivo and does so, at least in part, by promoting the destruction of c-JUN. These findings challenge the view that COP1 regulates p53 stability and call into question the wisdom of developing COP1 inhibitors as potential anticancer agents.

Indexed as

AnimalsEnzyme StabilityHumansJNK Mitogen-Activated Protein KinasesMiceMice, Mutant StrainsModels, BiologicalNeoplasmsNuclear ProteinsTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin-Protein LigasesCOP1 protein, mouseJNK Mitogen-Activated Protein KinasesNuclear ProteinsTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID21403396
PMCPMC3069793
OpenAlexW2134252799

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.