ArticlePloS one2011
Characterisation of a C1qtnf5 Ser163Arg knock-in mouse model of late-onset retinal macular degeneration.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Distinct Phenotypic Consequences of Pathogenic Mutants Associated with Late-Onset Retinal Degeneration.The American journal of pathology · 2023Article
- Proline metabolism and transport in retinal health and disease.Amino acids · 2021Review
- Late-onset retinal degeneration pathology due to mutations in CTRP5 is mediated through HTRA1.Aging cell · 2019Article
- Loss of CTRP5 improves insulin action and hepatic steatosis.American journal of physiology. Endocrinology and metabolism · 2016Article
- Pathological Effects of Mutant C1QTNF5 (S163R) Expression in Murine Retinal Pigment Epithelium.Investigative ophthalmology & visual science · 2015Article
- Article
- Presence of rd8 mutation does not alter the ocular phenotype of late-onset retinal degeneration mouse model.Molecular vision · 2015Article
- Metabolic function of the CTRP family of hormones.Reviews in endocrine & metabolic disorders · 2014Review
- Differential modulation of retinal degeneration by Ccl2 and Cx3cr1 chemokine signalling.PloS one · 2012Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
A single founder mutation resulting in a Ser163Arg substitution in the C1QTNF5 gene product causes autosomal dominant late-onset retinal macular degeneration (L-ORMD) in humans, which has clinical and pathological features resembling age-related macular degeneration. We generated and characterised a mouse "knock-in" model carrying the Ser163Arg mutation in the orthologous murine C1qtnf5 gene by site-directed mutagenesis and homologous recombination into mouse embryonic stem cells. Biochemical, immunological, electron microscopic, fundus autofluorescence, electroretinography and laser photocoagulation analyses were used to characterise the mouse model. Heterozygous and homozygous knock-in mice showed no significant abnormality in any of the above measures at time points up to 2 years. This result contrasts with another C1qtnf5 Ser163Arg knock-in mouse which showed most of the features of L-ORMD but differed in genetic background and targeting construct.
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Registered trials
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