ArticleFEBS open bio2020
CANT1 deficiency in a mouse model of Desbuquois dysplasia impairs glycosaminoglycan synthesis and chondrocyte differentiation in growth plate cartilage.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- CANT1 as a novel prognostic biomarker in triple-negative breast cancer.Oncology letters · 2026Article
- Dysregulation of the Cant1/β-Catenin/TCF4-CHSY1 Axis Underpins Impaired ECM Biosynthesis in Skeletal Disorders.Research (Washington, D.C.) · 2026Article
- Genetic Association of CANT1 Gene with Scoliosis: An Integrative Study Involving Methylation, Immune Factors, and Metabolites.Journal of molecular neuroscience : MN · 2025Article
- CANT1 Is Involved in Collagen Fibrogenesis in Tendons by Regulating the Synthesis of Dermatan/Chondroitin Sulfate Attached to the Decorin Core Protein.International journal of molecular sciences · 2025Article
- Clinical and Molecular Cytogenetic Characterization of 2 Sibling Cases with 17q25 Duplication due to Unbalanced Translocation.Molecular syndromology · 2024Article
- Cant1 Affects Cartilage Proteoglycan Properties: Aggrecan and Decorin Characterization in a Mouse Model of Desbuquois Dysplasia Type 1.Biomolecules · 2024Article
- Article
- Integrated proteomics and metabolomics analysis of lumbar in a rat model of osteoporosis treated with Gushukang capsules.BMC complementary medicine and therapies · 2022Article
- Calcium-activated nucleotides 1 (CANT1)-driven nuclear factor-k-gene binding (NF-ĸB) signaling pathway facilitates the lung cancer progression.Bioengineered · 2022Article
- Mechanosensory and mechanotransductive processes mediated by ion channels in articular chondrocytes: Potential therapeutic targets for osteoarthritis.Channels (Austin, Tex.) · 2021Review
- Chondrodysplasias With Multiple Dislocations Caused by Defects in Glycosaminoglycan Synthesis.Frontiers in genetics · 2021Review
- An Overview ofFrontiers in cell and developmental biology · 2021Review
- Genome Editing for Rare Diseases.Current stem cell reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desbuquois dysplasia (DD) type 1 is a rare skeletal dysplasia characterized by a short stature, round face, progressive scoliosis, and joint laxity. The causative gene has been identified as calcium-activated nucleotidase 1 (CANT1), which encodes a nucleotidase that preferentially hydrolyzes UDP to UMP and phosphate. In this study, we generated Cant1 KO mice using CRISPR/Cas9-mediated genome editing. All F0 mice possessing frameshift deletions at both Cant1 alleles exhibited a dwarf phenotype. Germline transmission of the edited allele was confirmed in an F0 heterozygous mouse, and KO mice were generated by crossing of the heterozygous breeding pairs. Cant1 KO mice exhibited skeletal defects, including short stature, thoracic kyphosis, and delta phalanx, all of which are observed in DD type 1 patients. The glycosaminoglycan (GAG) content and extracellular matrix space were reduced in the growth plate cartilage of mutants, and proliferating chondrocytes lost their typical flat shape and became round. Chondrocyte differentiation, especially terminal differentiation to hypertrophic chondrocytes, was impaired in Cant1 KO mice. These findings indicate that CANT1 is involved in the synthesis of GAG and regulation of chondrocyte differentiation in the cartilage and contribute to a better understanding of the pathogenesis of DD type 1.
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