Evidence map›Paper›PMID 26934134›Full record

ArticleInvestigative ophthalmology & visual science2016

Role of RDS and Rhodopsin in Cngb1-Related Retinal Degeneration.

Dibyendu Chakraborty, Shannon M Conley, Steven J Pittler, Muna I Naash

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Deletion ofInternational journal of ophthalmology · 2021
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. C8ORF37 Is Required for Photoreceptor Outer Segment Disc Morphogenesis by Maintaining Outer Segment Membrane Protein Homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  8. 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

4 authors at 3 institutions in 1 country.

Dibyendu ChakrabortyDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.
Shannon M ConleyDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.
Steven J PittlerDepartment of Vision Sciences, School of Optometry, University of Alabama at Birmingham, Birmingham, Alabama, United States.
Muna I NaashDepartment of Biomedical Engineering, University of Houston, Houston, Texas, United States.
University of Oklahoma Health Sciences Center · USUniversity of Alabama at Birmingham · USUniversity of Houston · US

Funding

Visual Phenotyping CoreP30EY003039 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Paul Douglas Gamlin · 1985 to 2026
$16.9M
Supplement for: Mechanism of Photoreceptor Cell Degeneration in Animal Models of Retinal DiseasesR01EY010609 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MUAYYAD R AL-UBAIDI, Muna I. Naash · 1995 to 2026
$11.0M
Analysis of retina rod photoreceptor GARP and cGMP-gated channelR01EY018143 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PITTLER, STEVEN J · 2008 to 2016
$2.9M
NEI NIH HHS P30 EY003039NEI NIH HHS P30EY003039NEI NIH HHS R01 EY010609NEI NIH HHS R01EY010609NEI NIH HHS R01 EY018143NEI NIH HHS R01EY018143-06
6 · The paper itself

Abstract

purposeRod photoreceptor outer segment (OS) morphogenesis, structural integrity, and proper signal transduction rely on critical proteins found in the different OS membrane domains (e.g., plasma, disc, and disc rim membrane). Among these key elements are retinal degeneration slow (RDS, also known as peripherin-2), rhodopsin, and the beta subunit of the cyclic nucleotide gated channel (CNGB1a), which have been found to interact in a complex. The purpose of this study was to evaluate the potential interplay between these three proteins by examining retinal disease phenotypes in animal models expressing varying amounts of CNGB1a, rhodopsin, and RDS.

methodsOuter segment trafficking, retinal function, and photoreceptor structure were evaluated using knockout mouse lines.

resultsEliminating Cngb1 and reducing RDS leads to additive defects in RDS expression levels and rod electroretinogram (ERG) function, (e.g., Cngb1-/-/rds+/- versus rds+/- or Cngb1-/-) but not to additive defects in rod ultrastructure. These additive effects also manifested in cone function: Photopic ERG responses were significantly lower in the Cngb1-/-/rds+/- versus rds+/- or Cngb1-/-, suggesting that eliminating Cngb1 can accelerate the cone degeneration that usually presents later in the rds+/-. This was not the case with rhodopsin; reducing rhodopsin levels in concert with eliminating CNGB1a did not lead to phenotypes more severe than those observed in the Cngb1 knockout alone.

conclusionsThese data support a role for RDS as the core component of a multiprotein plasma membrane-rim-disc complex that has both a structural role in photoreceptor OS formation and maintenance and a functional role in orienting proteins for optimal signal transduction.

Indexed as

Gene Expression RegulationAnimalsCyclic Nucleotide-Gated Cation ChannelsElectroretinographyMiceMice, KnockoutMicroscopy, Electron, TransmissionNerve Tissue ProteinsPeripherinsRetinal Cone Photoreceptor CellsRetinal DegenerationRhodopsinRNACngb1 protein, mouseCyclic Nucleotide-Gated Cation ChannelsNerve Tissue ProteinsPeripherinsPrph2 protein, mouseRhodopsinRNA

Identifiers

PMID26934134
PMCPMC4777275
OpenAlexW2290949816

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.