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• W2073023239 abstract "The zinc transporter protein ZIP13 plays crucial roles in bone, tooth, and connective tissue development, and its dysfunction is responsible for the spondylocheirodysplastic form of Ehlers-Danlos syndrome (SCD-EDS, OMIM 612350). We recently reported that the pathogenic mutations in ZIP13 reduce its functional protein level by accelerating the protein degradation via the VCP-linked ubiquitin proteasome pathway, resulting in the disturbance of intracellular zinc homeostasis that appears to contribute to SCD-EDS pathogenesis. Finally, we implicate that possible therapeutic approaches for SCD-EDS would be based on regulating the degradation of the pathogenic mutant ZIP13 proteins." @default.
• W2073023239 created "2016-06-24" @default.
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• W2073023239 date "2014-01-01" @default.
• W2073023239 modified "2023-10-17" @default.
• W2073023239 title "Spondylocheirodysplastic Ehlers-Danlos syndrome (SCD-EDS) and the mutant zinc transporter ZIP13" @default.
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• W2073023239 doi "https://doi.org/10.4161/21675511.2014.974982" @default.
• W2073023239 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4755239" @default.
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