Evidence map›Paper›PMID 15184660›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Knock-in human rhodopsin-GFP fusions as mouse models for human disease and targets for gene therapy.

Fung Chan, Allan Bradley, Theodore G Wensel, John H Wilson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

57 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Rhodopsin mislocalization drives ciliary dysregulation in a novel autosomal dominant retinitis pigmentosa knock-in mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. CRISPR genome surgery in a novel humanized model for autosomal dominant retinitis pigmentosa.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. In vivo mapping of a GPCR interactome using knockin mice.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. Humanising the mouse genome piece by piece.Nature communications · 2019
    Review
  18. A Novel Mouse Model ofFrontiers in neuroscience · 2019
    Article
  19. Article
  20. Review
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 1 institution in 1 country.

Fung ChanVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
Allan Bradley
Theodore G Wensel
John H Wilson
Baylor College of Medicine · US

Funding

VISION RESEARCH CENTERP30EY002520 · NEI · BAYLOR COLLEGE OF MEDICINE · PI Samuel M Wu · 1985 to 2026
$14.8M
RHODOSPIN GENE CORRECTION BY OLIGONUCLEOTIDE TARGETINGR01EY011731 · NEI · BAYLOR COLLEGE OF MEDICINE · PI WILSON, JOHN H · 1997 to 2014
$5.9M
NEI NIH HHS EY002520NEI NIH HHS EY11731NEI NIH HHS P30 EY002520NEI NIH HHS R01 EY011731
6 · The paper itself

Abstract

The human rhodopsin gene is the locus for numerous alleles linked to the neurodegenerative disease retinitis pigmentosa. To facilitate the study of retinal degeneration and to test reagents designed to alter the structure and function of this gene, we have developed strains of mice whose native rhodopsin gene has been replaced with the corresponding human DNA modified to encode an enhanced GFP fusion at the C terminus of rhodopsin. The human rhodopsin-GFP fusion faithfully mimics the expression and distribution of wild-type rhodopsin in heterozygotes and serves as a sensitive reporter of rod-cell structure and integrity. In homozygotes, however, the gene induces progressive retinal degeneration bearing many of the hallmarks of recessive retinitis pigmentosa. When the gene is flanked by recognition sites for Cre recombinase, protein expression is reduced approximately 5-fold despite undiminished mRNA levels, suggesting translation inhibition. GFP-tagged human rhodopsin provides a sensitive method to monitor the development of normal and diseased retinas in dissected samples, and it offers a noninvasive means to observe the progress of retinal degeneration and the efficacy of gene-based therapies in whole animals.

Indexed as

AnimalsAnimals, Genetically ModifiedBlastocystCell NucleusCell SurvivalDisease Models, AnimalGene ExpressionGenetic TherapyGreen Fluorescent ProteinsHumansLuminescent ProteinsMaleMiceRecombinant Fusion ProteinsRetinaRetinal DegenerationGreen Fluorescent ProteinsLuminescent ProteinsRecombinant Fusion ProteinsRhodopsin

Identifiers

PMID15184660
PMCPMC428481
OpenAlexW2027714126

What OpenQuestion holds

Textmetadata
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.