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Proteome analysis of the retina from RhoQ344X/+ mouse

ABSTRACT: Retinal proteomes from wild-type and RhoQ344X mutant mice at postnatal day 35 were analyzed by label-free quantitative proteomics to understand proteomic change caused by the rhodopsin mutation.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Yoshikazu Imanishi

PROVIDER: MSV000093339 | MassIVE | Wed Nov 08 15:02:00 GMT 2023

SECONDARY ACCESSION(S): PXD046795

REPOSITORIES: MassIVE

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Rhodopsin mislocalization drives ciliary dysregulation in a novel autosomal dominant retinitis pigmentosa knock-in mouse model.

Takita Shimpei S Jahan Sultana S S Imanishi Sanae S Harikrishnan Hemavathy H LePage David D Mann Rachel J RJ Conlon Ronald A RA Miyagi Masaru M Imanishi Yoshikazu Y

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20240401 8

Rhodopsin mislocalization encompasses various blind conditions. Rhodopsin mislocalization is the primary factor leading to rod photoreceptor dysfunction and degeneration in autosomal dominant retinitis pigmentosa (adRP) caused by class I mutations. In this study, we report a new knock-in mouse model that harbors a class I Q344X mutation in the endogenous rhodopsin gene, which causes rod photoreceptor degeneration in an autosomal dominant pattern. In Rho<sup>Q344X/+</sup> mice, mRNA transcripts f ...[more]

PMID: 38648465

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