Evidence map›Paper›PMID 21876386›Full record

ReviewCell cycle (Georgetown, Tex.)2011

Roles of COP9 signalosome in cancer.

Mong-Hong Lee, Ruiying Zhao, Liem Phan, Sai-Ching J Yeung

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
4.3field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. The emerging roles of Jab1/CSN5 in cancer.Medical oncology (Northwood, London, England) · 2016
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. COPS6 promotes tumor progression and reduces CD8Acta pharmacologica Sinica · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Adaptive exchange sustains cullin-RING ubiquitin ligase networks and proper licensing of DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

25 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

4 authors at 1 institution in 1 country.

Mong-Hong LeeThe University of Texas MD Anderson Cancer Center, Houston, TX, USA. mhlee@mdanderson.org
Ruiying Zhao
Liem Phan
Sai-Ching J Yeung
The University of Texas MD Anderson Cancer Center · US

Funding

Regulation of cyclin-dependent kinase inhibitor p27 in cancerR01CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2002 to 2013
$2.8M
Regulation of cyclin-dependent kinase inhibitor p27 in cancerR56CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2008 to 2008
$276k
NCI NIH HHS R01 CA089266NCI NIH HHS R01CA 089266NCI NIH HHS R56 CA089266
6 · The paper itself

Abstract

The constitutive photomorphogenesis 9 signalosome (COP9 or CSN) is an evolutionarily conserved multiprotein complex found in plants and animals. Because of the homology between the COP9 signalosome and the 19S lid complex of the proteosome, COP9 has been postulated to play a role in regulating the degradation of polyubiquitinated proteins. Many tumor suppressor and oncogene products are regulated by ubiquitination- and proteosome-mediated protein degradation. Therefore, it is conceivable that COP9 plays a significant role in cancer, regulating processes relevant to carcinogenesis and cancer progression (e.g., cell cycle control, signal transduction and apoptosis). In mammalian cells, it consists of eight subunits (CSN1 to CSN8). The relevance and importance of some subunits of COP9 to cancer are emerging. However, the mechanistic regulation of each subunit in cancer remains unclear. Among the CSN subunits, CSN5 and CSN6 are the only two that each contain an MPN (Mpr1p and Pad1p N-terminal) domain. The deneddylation activity of an MPN domain toward cullin-RING ubiquitin ligases (CRL) may coordinate CRL-mediated ubiquitination activity. More recent evidence shows that CSN5 and CSN6 are implicated in ubiquitin-mediated proteolysis of important mediators in carcinogenesis and cancer progression. Here, we discuss the mechanisms by which some CSN subunits are involved in cancer to provide a much needed perspective regarding COP9 in cancer research, hoping that these insights will lay the groundwork for cancer intervention.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Transformation, NeoplasticCOP9 Signalosome ComplexCullin ProteinsCyclin-Dependent Kinase Inhibitor p27DNA DamageHaploinsufficiencyHumansIntracellular Signaling Peptides and ProteinsMammalsMiceMice, KnockoutMultiprotein ComplexesNeoplasmsOncogenesCOP9 Signalosome ComplexCOPS5 protein, humanCullin ProteinsCyclin-Dependent Kinase Inhibitor p27Intracellular Signaling Peptides and ProteinsMdm2 protein, mouseMultiprotein ComplexesPeptide HydrolasesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID21876386
PMCPMC3218617
OpenAlexW1966396139

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.