ArticleBiochimica et biophysica acta. Molecular basis of disease2019
Inactivation of FAM20B causes cell fate changes in annulus fibrosus of mouse intervertebral disc and disc defects via the alterations of TGF-β and MAPK signaling pathways.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Causal neurodevelopmental origins of scoliosis: Multi-omics Mendelian randomization reveals brain-region-specific pathways and protein mediators.Journal of orthopaedic translation · 2026Article
- FAM20B-Catalyzed Glycosylation Regulates the Chondrogenic and Osteogenic Differentiation of the Embryonic Condyle by Controlling IHH Diffusion and Release.International journal of molecular sciences · 2025Article
- Exploring the Causes of Intervertebral Disc Annulus Fibrosus Impairment.Cellular and molecular bioengineering · 2025Review
- Crosslinking stabilization strategy: A novel approach to cartilage-like repair of annulus fibrosus (AF) defects.Materials today. Bio · 2025Article
- Systems genetics uncover new loci containing functional gene candidates in Mycobacterium tuberculosis-infected Diversity Outbred mice.PLoS pathogens · 2024Article
- The JNK signaling pathway in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024Review
- Systems genetics uncover new loci containing functional gene candidates inbioRxiv : the preprint server for biology · 2023Article
- Review
- Deficiency ofInternational journal of molecular sciences · 2023Article
- Review
- Regulation of secretory pathway kinase or kinase-like proteins in human cancers.Frontiers in immunology · 2023Review
- Unraveling the mechanisms of intervertebral disc degeneration: an exploration of the p38 MAPK signaling pathway.Frontiers in cell and developmental biology · 2023Review
- An Overview ofFrontiers in cell and developmental biology · 2021Review
- Chondrodysplasias With Multiple Dislocations Caused by Defects in Glycosaminoglycan Synthesis.Frontiers in genetics · 2021Review
- Heparan Sulfate Biosynthesis in Zebrafish.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Review
- Ablation of Fam20c causes amelogenesis imperfecta via inhibiting Smad dependent BMP signaling pathway.Biology direct · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Intervertebral disc (IVD) disorder is often caused by the defect of annulus fibrosus (AF), especially that of the outer AF. Studies about the mechanisms governing the development of the outer AF are needed for a better understanding of pathogenesis of IVD defects. Glycosaminoglycans (GAGs) are essential components of extracellular matrix (ECM) in AF. FAM20B is a newly identified xylose kinase that catalyzes the biosynthesis of GAGs. In this study, we created Fam20B conditional knockout (cKO) mice in which FAM20B was inactivated in type I collagen-expressing cells, the main type of cells in the outer AF of IVD. The cKO mice showed severe spine deformity and remarkable IVD defects associated with AF malformation. The AF of cKO mice had a lower level of chondroitin sulfate and heparan sulfate, and the outer AF cells lost their normal fibroblast-like morphology and acquired chondrocyte phenotypes, expressing a higher level of Sox 9 and type II collagen along with a reduced level of type I collagen. The level of phospho-Smad 2 and phospho-Smad 3, and that of scleraxis, a downstream target molecule of canonical TGF-β signaling pathway were significantly lower in the AF of cKO mice. The AF in cKO mice also manifested altered levels in the molecules associated with the activations of MAPK pathway; the changes included the increase of phospho-P38 and phospho-ERK and a decrease of phospho-JNK. These results indicate that FAM20B plays an essential role in the development of AF by regulating the TGF-β signaling and MAPK signaling pathways.
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