Evidence map›Paper›PMID 22673153›Full record

ReviewNature reviews. Cancer2012

Spotlight on the role of COP1 in tumorigenesis.

Jean-Christophe Marine

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

74 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
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  12. p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  13. Article
  14. Article
  15. Article
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  17. COP1 controls light-dependent chromatin remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Review
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Jean-Christophe MarineLaboratory for Molecular Cancer Biology, VIB-KULeuven, O&N I Herestraat 49, Leuven, Belgium. JeanChristophe.Marine@cme.vib-kuleuven.be
VIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COP1 is an E3 ubiquitin ligase that is involved in the ubiquitylation of various protein substrates to trigger their proteasomal degradation. Although originally identified in a light signalling pathway in plants, biochemical studies have identified putative targets of mammalian COP1 with relevant roles in tumorigenesis, including the oncoproteins JUN and ETV family members, as well as the p53 tumour suppressor. Recent genetic studies have shown that COP1 deficiency leads to spontaneous tumour formation in mice, and have identified mutations in COP1 and its substrates in various human cancers. These findings add to our growing appreciation of the roles for E3 ligases in cancer.

Indexed as

AnimalsCell Transformation, NeoplasticHumansMiceOncogene ProteinsSignal TransductionTumor Suppressor ProteinsUbiquitinationUbiquitin-Protein LigasesCOP1 protein, humanOncogene ProteinsTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID22673153
OpenAlexW2085013798

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.