ArticleMatrix biology : journal of the International Society for Matrix Biology2019
Calcium activated nucleotidase 1 (CANT1) is critical for glycosaminoglycan biosynthesis in cartilage and endochondral ossification.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 51 citations in OpenAlex.
- First Thai Case of Lethal Desbuquois Dysplasia Type I Caused by Novel Compound HeterozygousCase reports in genetics · 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
- Genetic variability in proteoglycan biosynthetic genes reveals new facets of heparan sulfate diversity.Essays in biochemistry · 2024Review
- Clinical and Molecular Cytogenetic Characterization of 2 Sibling Cases with 17q25 Duplication due to Unbalanced Translocation.Molecular syndromology · 2024Article
- Clinical and Genetic Insights into Desbuquois Dysplasia: Review of 111 Case Reports.International journal of molecular sciences · 2024Review
- Cant1 Affects Cartilage Proteoglycan Properties: Aggrecan and Decorin Characterization in a Mouse Model of Desbuquois Dysplasia Type 1.Biomolecules · 2024Article
- Identification of Candidate Genes for Economically Important Carcass Cutting in Commercial Pigs through GWAS.Animals : an open access journal from MDPI · 2023Article
- Circ_0001715 accelerated lung adenocarcinoma process by the miR-1322/CANT1 axis.Diagnostic pathology · 2023Article
- Comprehensive multi-omic profiling of somatic mutations in malformations of cortical development.Nature genetics · 2023Article
- Calcium-activated nucleotides 1 (CANT1)-driven nuclear factor-k-gene binding (NF-ĸB) signaling pathway facilitates the lung cancer progression.Bioengineered · 2022Article
- Review
- Phenotypic Characterization of Immortalized Chondrocytes from a Desbuquois Dysplasia Type 1 Mouse Model: A Tool for Studying Defects in Glycosaminoglycan Biosynthesis.International journal of molecular sciences · 2021Article
- Extracellular matrix: an important regulator of cell functions and skeletal muscle development.Cell & bioscience · 2021Review
- Chondrodysplasias With Multiple Dislocations Caused by Defects in Glycosaminoglycan Synthesis.Frontiers in genetics · 2021Review
- An Overview ofFrontiers in cell and developmental biology · 2021Review
- Single-Cell Integration Analysis of Heterotopic Ossification and Fibrocartilage Developmental Lineage: Endoplasmic Reticulum Stress Effector Xbp1 Transcriptionally Regulates the Notch Signaling Pathway to Mediate Fibrocartilage Differentiation.Oxidative medicine and cellular longevity · 2021Article
- Cloning, expression and enzyme activity delineation of two novel CANT1 mutations: the disappearance of dimerization may indicate the change of protein conformation and even function.Orphanet journal of rare diseases · 2020Article
- Identifying the pattern of immune related cells and genes in the peripheral blood of ischemic stroke.Journal of translational medicine · 2020Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desbuquois dysplasia type 1 (DBQD1) is a chondrodysplasia caused by mutations in CANT1 gene encoding an ER/Golgi calcium activated nucleotidase 1 that hydrolyses UDP. Here, using Cant1 knock-in and knock-out mice recapitulating DBQD1 phenotype, we report that CANT1 plays a crucial role in cartilage proteoglycan synthesis and in endochondral ossification. Specifically, the glycosaminoglycan synthesis was decreased in chondrocytes from Cant1 knock-out mice and their hydrodynamic size was reduced, whilst the sulfation was increased and the overall proteoglycan secretion was delayed. Interestingly, knock-out chondrocytes had dilated ER cisternae suggesting delayed protein secretion and cellular stress; however, no canonical ER stress response was detected using microarray analysis, Xbp1 splicing and protein levels of BiP and ATF4. The observed proteoglycan defects caused deregulated chondrocyte proliferation and maturation in the growth plate resulting in the reduced skeletal growth. In conclusion, the pathogenic mechanism of DBQD1 comprises deregulated chondrocyte performance due to defective intracellular proteoglycan synthesis and altered proteoglycan properties in the extracellular matrix.
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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.