ArticleExperimental animals2019
Mice harboring an MCTO mutation exhibit renal failure resembling nephropathy in human patients.
Article in Experimental animals, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Inhibition of MAFB and PI3K/AKT Signaling for Hereditary FSGS with Multicentric Carpotarsal Osteolysis.Journal of the American Society of Nephrology : JASN · 2026Article
- Mycobacterium tuberculosis impairs protective cytokine production via transcription factor MafB manipulation.PLoS pathogens · 2025Article
- Exploring Large MAF Transcription Factors: Functions, Pathology, and Mouse Models with Point Mutations.Genes · 2023Review
- Denosumab Treatment Does Not Halt Progression of Bone Lesions in Multicentric Carpotarsal Osteolysis Syndrome.JBMR plus · 2023Article
- Multicentric Carpotarsal Osteolysis: a Contemporary Perspective on the Unique Skeletal Phenotype.Current osteoporosis reports · 2023Review
- Podocyte-specific Transcription Factors: Could MafB Become a Therapeutic Target for Kidney Disease?Internal medicine (Tokyo, Japan) · 2023Review
- ZebrafishBiomolecules · 2021Article
- Role of MafB in macrophages.Experimental animals · 2020Review
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multicentric carpotarsal osteolysis (MCTO) is a condition involving progressive osteolysis of the carpal and tarsal bones that is associated with glomerular sclerosis and renal failure (MCTO nephropathy). Previous work identified an autosomal dominant missense mutation in the transactivation domain of the transcription factor MAFB as the cause of MCTO. Several methods are currently used for MCTO nephropathy treatment, but these methods are invasive and lead to severe side effects, limiting their use. Therefore, the development of alternative treatments for MCTO nephropathy is required; however, the pathogenesis of MCTO in vivo is unclear without access to a mouse model. Here, we report the generation of an MCTO mouse model using the CRISPR/Cas9 system. These mice exhibit nephropathy symptoms that are similar to those observed in MCTO patients. Mafb
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