Evidence map›Paper›PMID 21992067›Full record

ArticleThe Biochemical journal2012

Defective trafficking of cone photoreceptor CNG channels induces the unfolded protein response and ER-stress-associated cell death.

Deborah L Duricka, R Lane Brown, Michael D Varnum

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  17. Neuroprotective strategies for retinal disease.Progress in retinal and eye research · 2018
    Review
  18. Article
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  20. Article
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.

Deborah L DurickaDepartment of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164, USA.
R Lane Brown
Michael D Varnum
Washington State University · US

Funding

Molecular Mechanisms of Retinal cGMP-Activated Ion ChannelsR01EY012836 · NEI · WASHINGTON STATE UNIVERSITY · PI VARNUM, MICHAEL D. · 2000 to 2012
$3.4M
TRP channel expression and function in ON-bipolar cellsR01EY019907 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BROWN, RONALD LANE, DUVOISIN, ROBERT M · 2010 to 2012
$1.4M
NEI NIH HHS EY12836NEI NIH HHS EY19907NEI NIH HHS R01 EY012836NEI NIH HHS R01 EY019907
6 · The paper itself

Abstract

Mutations that perturb the function of photoreceptor CNG (cyclic nucleotide-gated) channels are associated with several human retinal disorders, but the molecular and cellular mechanisms leading to photoreceptor dysfunction and degeneration remain unclear. Many loss-of-function mutations result in intracellular accumulation of CNG channel subunits. Accumulation of proteins in the ER (endoplasmic reticulum) is known to cause ER stress and trigger the UPR (unfolded protein response), an evolutionarily conserved cellular programme that results in either adaptation via increased protein processing capacity or apoptotic cell death. We hypothesize that defective trafficking of cone photoreceptor CNG channels can induce UPR-mediated cell death. To test this idea, CNGA3 subunits bearing the R563H and Q655X mutations were expressed in photoreceptor-derived 661W cells with CNGB3 subunits. Compared with wild-type, R563H and Q655X subunits displayed altered degradation rates and/or were retained in the ER. ER retention was associated with increased expression of UPR-related markers of ER stress and with decreased cell viability. Chemical and pharmacological chaperones {TUDCA (tauroursodeoxycholate sodium salt), 4-PBA (sodium 4-phenylbutyrate) and the cGMP analogue CPT-cGMP [8-(4-chlorophenylthio)-cGMP]} differentially reduced degradation and/or promoted plasma-membrane localization of defective subunits. Improved subunit maturation was concordant with reduced expression of ER-stress markers and improved viability of cells expressing localization-defective channels. These results indicate that ER stress can arise from expression of localization-defective CNG channels, and may represent a contributing factor for photoreceptor degeneration.

Indexed as

AnimalsCell DeathCell LineCell MembraneCyclic GMPCyclic Nucleotide-Gated Cation ChannelsEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHumansMiceMolecular ChaperonesProtein TransportRetinal Cone Photoreceptor CellsTranscription Factor CHOPUnfolded Protein ResponseCNGA3 protein, humanCPT-cGMPCyclic GMPCyclic Nucleotide-Gated Cation ChannelsDdit3 protein, mouseEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMolecular ChaperonesTranscription Factor CHOP

Identifiers

PMID21992067
PMCPMC3257030
OpenAlexW2144209376

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.