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Proteomic characterization of infant and adult ornithine aminotransferase-deficient mice

ABSTRACT: The deficiency of ornithine aminotransferase (OAT) cause gyrate atrophy, a progressive chorioretinal degeneration disease culminating in blindness. This project investigates age- and tissue-specific proteomic changes in the retina, retinal pigment epithelium (RPE), and liver of OAT-deficient mice to uncover the role of the enzyme in these tissues and the mechanisms underlying the eye damage.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Retinal Pigment Epithelium Cell Line, Liver, Retina

SUBMITTER: Dennis Province

LAB HEAD: Jianhai Du

PROVIDER: PXD063614 | Pride | 2026-07-06

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	2023_02_UniProt_Mus_musculus.fasta	Fasta
	DuJ_061423_GPF6_Liver_1.mgf	Mgf
	DuJ_061423_GPF6_Liver_1.raw	Raw
	DuJ_061423_GPF6_Liver_2.mgf	Mgf
	DuJ_061423_GPF6_Liver_2.raw	Raw

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Publications

Early proteomic and metabolic signatures of liver and eye in OAT-deficient mice.

Puja Artjola A Xu Rong R Mascari Isabella I Ngo Tuan T Zhang Ying Y Wang Qingyan Q Saravanan Meghashri M Du Jianhai J

Experimental eye research 20260629

Ornithine aminotransferase (OAT) deficiency causes hyperornithinemia and gyrate atrophy (GA) of the choroid and retina, a rare inherited retinal degeneration. To understand the early molecular changes that make the eye susceptible to damage, we performed quantitative proteomic and metabolomic profiling of liver, retina, and retinal pigment epithelium and choroid (RPE/Cho) from OAT-deficient (Oat<sup>rhg</sup>) mice prior to detectable vision impairment. In addition to reduced OAT expression and ...[more]

PMID: 42373003

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