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Article

Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration

1 May 2000

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Share to Photoreceptor and optogenetics research
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Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 10802658
DOI: 10.1038/75614

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Related research

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Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degenerationPMID 10802658Read ↗

Rpe65 is necessary for production of 11-cis-vitamin A in the retinal visual cycle.Semantic proximity Read ↗

New views on RPE65 deficiency: the rod system is the source of vision in a mouse model of Leber congenital amaurosisSemantic proximity Read ↗

<i>RPE65</i> knockout <i>Xenopus laevis</i> have a compromised but detectable electroretinogram and altered visual responses, without retinal degeneration or altered melanophore dispersionSemantic proximity Read ↗

RPE Visual Cycle and Biochemical Phenotypes of Mutant Mouse Models.Semantic proximity Read ↗

Nonvisual light responses in the Rpe65 knockout mouse: rod loss restores sensitivity to the melanopsin system.Semantic proximity Read ↗

Retinal disease in Rpe65-deficient mice: comparison to human leber congenital amaurosis due to RPE65 mutations.Semantic proximity Read ↗

An inducible Cre mouse for studying roles of the RPE in retinal physiology and diseaseSemantic proximity Read ↗

Environmental Light Has an Essential Effect on the Disease Expression in a Dominant RPE65 Mutation.Semantic proximity Read ↗

R91W mutation in Rpe65 leads to milder early-onset retinal dystrophy due to the generation of low levels of 11-cis-retinalSemantic proximity Read ↗

A Mild Form of RPE65-Associated Retinopathy.Semantic proximity Read ↗

Rpe65 as a modifier gene for inherited retinal degeneration.Semantic proximity Read ↗

In conditions of limited chromophore supply rods entrap 11-cis-retinal leading to loss of cone function and cell death.Semantic proximity Read ↗

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