Evidence map›Paper›PMID 38365903›Full record

ArticleNature communications2024

Aggregation of rhodopsin mutants in mouse models of autosomal dominant retinitis pigmentosa.

Sreelakshmi Vasudevan, Subhadip Senapati, Maryanne Pendergast, Paul S-H Park

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. RNA interference to reduceMolecular vision · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Aggregation of the Constitutively Active K296E Rhodopsin Mutant Contributes to Retinal Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Article
  12. Article
  13. Molecular therapy. Nucleic acids · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. 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 2 institutions in 1 country.

Sreelakshmi VasudevanDepartment of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA.ORCID 0000-0001-9534-4559
Subhadip SenapatiDepartment of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA.ORCID 0000-0001-9071-1911
Maryanne PendergastDepartment of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA.
Paul S-H ParkDepartment of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA. paul.park@case.edu.ORCID 0000-0002-1638-9693
Case Western Reserve University · USPropagation Research Associates (United States) · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Clinical and Translational Science Collaborative of Northern Ohio, Catalyzing Linkages to Equity in Health (CLE Health)UM1TR004528 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI GRACE A MCCOMSEY · 2023 to 2026
$32.1M
TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
PHOTOTRANSDUCTION IN HEALTH AND DISEASE - Administrative SupplementR01EY021731 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Paul S Park · 2011 to 2026
$6.5M
Acquisition of a Leica TCS SP5 Confocal Microscope For A Multi-User FacilityS10OD016164 · OD · CASE WESTERN RESERVE UNIVERSITY · PI CONRAD, PATRICIA A · 2013 to 2013
$597k
NCATS NIH HHS UM1 TR004528NCRR NIH HHS UL1 RR024989NEI NIH HHS P30 EY011373NEI NIH HHS R01 EY021731NIH HHS S10 OD016164
6 · The paper itself

Abstract

Mutations in rhodopsin can cause it to misfold and lead to retinal degeneration. A distinguishing feature of these mutants in vitro is that they mislocalize and aggregate. It is unclear whether or not these features contribute to retinal degeneration observed in vivo. The effect of P23H and G188R misfolding mutations were examined in a heterologous expression system and knockin mouse models, including a mouse model generated here expressing the G188R rhodopsin mutant. In vitro characterizations demonstrate that both mutants aggregate, with the G188R mutant exhibiting a more severe aggregation profile compared to the P23H mutant. The potential for rhodopsin mutants to aggregate in vivo was assessed by PROTEOSTAT, a dye that labels aggregated proteins. Both mutants mislocalize in photoreceptor cells and PROTEOSTAT staining was detected surrounding the nuclei of photoreceptor cells. The G188R mutant promotes a more severe retinal degeneration phenotype and greater PROTEOSTAT staining compared to that promoted by the P23H mutant. Here, we show that the level of PROTEOSTAT positive cells mirrors the progression and level of photoreceptor cell death, which suggests a potential role for rhodopsin aggregation in retinal degeneration.

Indexed as

Retinal DegenerationRetinitis PigmentosaRhodopsinAnimalsDisease Models, AnimalMiceMutationPhotoreceptor CellsProtein AggregatesProtein AggregatesRhodopsin

Identifiers

PMID38365903
PMCPMC10873427
OpenAlexW4391876241

What OpenQuestion holds

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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.