Evidence map›Paper›PMID 18706515›Full record

ArticleThe international journal of biochemistry & cell biology2009

The COP9 signalosome negatively regulates proteasome proteolytic function and is essential to transcription.

Huabo Su, Wei Huang, Xuejun Wang

Abstract read
In one paragraph

Article in The international journal of biochemistry & cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding.American journal of physiology. Renal physiology · 2020
    Review
  3. Review
  4. Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling Pathway.Journal of the American Society of Nephrology : JASN · 2018
    Article
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  15. Article
  16. Enhancement of proteasome function by PA28α overexpression protects against oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
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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.

Huabo SuDivision of Basic Biomedical Sciences and Cardiovascular Research Institute, Sanford School of Medicine of the University of South Dakota, Vermillion, SD 57069, USA.
Wei Huang
Xuejun Wang
University of South Dakota · US

Funding

Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01HL085629
6 · The paper itself

Abstract

The COP9 signalosome (CSN) is an evolutionarily conserved protein complex formed by eight subunits (CSN1 through CSN8). Deneddylating cullin family proteins is considered the bona fide function of the CSN. It has been proposed that the CSN regulates the assembly and disassembly of the cullin-based ubiquitin ligases via its deneddylation activity. Here we report that down-regulation of CSN8 by RNA interference destabilized differentially other CSN subunits and reduced the amount of CSN holo-complexes, leading to increases in neddylated cullin proteins and reduction of F-box protein Skp2 in HEK293 cells. Moreover, suppression of CSN8 enhanced the degradation of a proteasome surrogate substrate and cyclin kinase inhibitor p21(cip). Reduced transcript levels of cyclin kinase inhibitor p21(cip) and p27(kip) were also observed upon down-regulation of CSN8. These data suggest that the homeostatic level of CSN8/CSN suppresses proteasome proteolytic function and regulates transcription.

Indexed as

AnimalsCarrier ProteinsCell Line, TumorCentral Nervous SystemCOP9 Signalosome ComplexCullin ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Down-RegulationF-Box ProteinsMiceMultiprotein ComplexesPeptide HydrolasesProtein MultimerizationRNA, Small InterferingS-Phase Kinase-Associated ProteinsCarrier ProteinsCdkn1a protein, mouseCOP9 Signalosome ComplexCops8 protein, mouseCullin ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27F-Box ProteinsMultiprotein ComplexesPeptide HydrolasesRNA, Small InterferingS-Phase Kinase-Associated Proteins

Identifiers

PMID18706515
PMCPMC2628451
OpenAlexW2005870945

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.