Evidence map›Paper›PMID 41338991›Full record

ArticleExperimental animals2026

A nonsense mutation in the Mocos gene induces xanthinuria, obstructive nephropathy, and anemia in rats.

Mao Urasaki, Kana Nagasaka, Minori Kido, Kenta Hayashi, Ayumi Watanabe, Kosuke Hattori, Takahiro Sekiguchi, Mitsuru Kuwamura, Miyuu Tanaka, Tomoji Mashimo and 1 more

Abstract read
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Article in Experimental animals, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

11 authors.

Mao UrasakiLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.
Kana NagasakaLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.
Minori KidoLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.
Kenta HayashiLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.
Ayumi WatanabeLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.
Kosuke HattoriDivision of Animal Genetics, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shiroganedai, Minato-ku, Tokyo 108-8639, Japan.
Takahiro SekiguchiLaboratory of Veterinary Pathology, Graduate School of Veterinary Science, Osaka Metropolitan University, 1-58 Rinku, Izumisano, Osaka 598-8531, Japan.
Mitsuru KuwamuraLaboratory of Veterinary Pathology, Graduate School of Veterinary Science, Osaka Metropolitan University, 1-58 Rinku, Izumisano, Osaka 598-8531, Japan.
Miyuu TanakaLaboratory of Veterinary Pathology, Graduate School of Veterinary Science, Osaka Metropolitan University, 1-58 Rinku, Izumisano, Osaka 598-8531, Japan.
Tomoji MashimoDivision of Animal Genetics, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shiroganedai, Minato-ku, Tokyo 108-8639, Japan.
Takashi KuramotoLaboratory of Animal Nutrition, Department of Animal Science, Faculty of Agriculture, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa 243-0034, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Xanthinuria type II is a rare hereditary disorder caused by mutations in the MOCOS gene, leading to dual deficiency of xanthine dehydrogenase and aldehyde oxidase. To establish a robust animal model for this condition, we generated Mocos knock-in (KI) rats carrying the Arg419Ter nonsense mutation identified in Japanese patients. Homozygous KI rats exhibited severe growth retardation, anemia, and reduced survival, with all individuals dying by 14 weeks of age. Biochemical analyses revealed elevated levels of hypoxanthine and xanthine, along with decreased uric acid in both serum and urine, confirming xanthinuria. Homozygous KI rats also showed increased blood creatinine (CRE) and urea nitrogen (UN), and decreased urinary CRE and UN, indicating renal dysfunction. Histopathological examination showed obstructive nephropathy characterized by tubular atrophy, crystal deposition, and inflammation. Compared to existing mouse models, Mocos KI rats demonstrated extended lifespan, enabling more detailed investigation of disease mechanisms. This rat model provides a valuable tool for studying the pathogenesis of xanthinuria type II and exploring potential therapeutic strategies.

Indexed as

Aldehyde OxidaseAnemiaCodon, NonsenseDisease Models, AnimalXanthine DehydrogenaseAnimalsGene Knock-In TechniquesHomozygoteMaleRatsXanthineAldehyde OxidaseCodon, NonsenseXanthineXanthine DehydrogenaseanemiaMocosnephropathyratsxanthinuria

Identifiers

PMID41338991
PMCPMC13100697

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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.