A congenic C57BL/6J rd1 mouse model for retinal degeneration research.

Laurel C Chandler, Apolonia Gardner, Constance L Cepko

Abstract read

In one paragraph

Article in Experimental eye research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

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

1 citing paper in PubMed.

Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.Journal of neurochemistry · 2026
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.

Laurel C ChandlerDepartments of Genetics and Ophthalmology, Blavatnik Institute, Harvard Medical School, Boston, MA, 02115, USA; Howard Hughes Medical Institute, Chevy Chase, MD, 20815, USA.

Apolonia GardnerDepartments of Genetics and Ophthalmology, Blavatnik Institute, Harvard Medical School, Boston, MA, 02115, USA; Virology Program, Harvard Medical School, Boston, MA, 02115, USA; Howard Hughes Medical Institute, Chevy Chase, MD, 20815, USA.

Constance L CepkoDepartments of Genetics and Ophthalmology, Blavatnik Institute, Harvard Medical School, Boston, MA, 02115, USA; Howard Hughes Medical Institute, Chevy Chase, MD, 20815, USA. Electronic address: cepko@genetics.med.harvard.edu.

Funding

Howard Hughes Medical Institute

6 · The paper itself

Abstract

Retinitis pigmentosa is an inherited retinal disease caused by thousands of mutations in over 100 different genes. The most widely used mouse model for retinitis pigmentosa has the retinal degeneration 1 (rd1) mutation in the Pde6b gene, which elicits rapid retinal degeneration and vision loss. A major limitation of these models is that these rd1 strains are not congenic, which prevents the use of appropriate controls. Furthermore, many strains have mutations in other genes which introduces genetic variability and may confound results. To address this issue, we backcrossed the rd1 allele from FVB mice onto a C57BL/6J genetic background over many generations, producing a C57BL/6J.Pde6b

Indexed as

Cyclic Nucleotide Phosphodiesterases, Type 6Disease Models, AnimalRetinal DegenerationRetinitis PigmentosaAnimalsElectroretinographyMiceMice, CongenicMice, Inbred C57BLMutationRetinaCyclic Nucleotide Phosphodiesterases, Type 6Pde6b protein, mouseC57BL/6J.Pde6b(rd1) strainC57BL/6J with rd1 mutationCongenicElectroretinogramInbredOptomotorPde6bRetinal degenerationRetinitis pigmentosaRods

Identifiers

PMID41380951

DOI10.1016/j.exer.2025.110804

PMCPMC13016136

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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.