Evidence map›Paper›PMID 26437438›Full record

ReviewBiomolecules2015

The Role of the COP9 Signalosome and Neddylation in DNA Damage Signaling and Repair.

Dudley Chung, Graham Dellaire

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

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  17. Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding.American journal of physiology. Renal physiology · 2020
    Review
  18. 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

2 authors at 1 institution in 1 country.

Dudley ChungDepartment of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada. dudleyc@dal.ca.
Graham DellaireDepartment of Pathology, Dalhousie University, Halifax, NS B3H 4R2, Canada. dellaire@dal.ca.
Dalhousie University · CA

Funding

Canadian Institutes of Health Research MOP-84260
6 · The paper itself

Abstract

The maintenance of genomic integrity is an important process in organisms as failure to sense and repair damaged DNA can result in a variety of diseases. Eukaryotic cells have developed complex DNA repair response (DDR) mechanisms to accurately sense and repair damaged DNA. Post-translational modifications by ubiquitin and ubiquitin-like proteins, such as SUMO and NEDD8, have roles in coordinating the progression of DDR. Proteins in the neddylation pathway have also been linked to regulating DDR. Of interest is the COP9 signalosome (CSN), a multi-subunit metalloprotease present in eukaryotes that removes NEDD8 from cullins and regulates the activity of cullin-RING ubiquitin ligases (CRLs). This in turn regulates the stability and turnover of a host of CRL-targeted proteins, some of which have established roles in DDR. This review will summarize the current knowledge on the role of the CSN and neddylation in DNA repair.

Indexed as

AnimalsCOP9 Signalosome ComplexDNA DamageDNA RepairHumansMultiprotein ComplexesPeptide HydrolasesProtein Processing, Post-TranslationalUbiquitinUbiquitinationCOP9 Signalosome ComplexMultiprotein ComplexesPeptide HydrolasesUbiquitinCOP9 SignalosomeDNA repairNEDD8

Identifiers

PMID26437438
PMCPMC4693240
OpenAlexW1671720437

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.