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Promotion of vesicular zinc efflux by ZIP13 and its implications for spondylocheiro dysplastic Ehlers–Danlos syndrome
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Promotion of vesicular zinc efflux by ZIP13 and its implications for spondylocheiro dysplastic Ehlers–Danlos syndrome
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Promotion of vesicular zinc efflux by ZIP13 and its implications for spondylocheiro dysplastic Ehlers–Danlos syndrome
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Journal Article
Promotion of vesicular zinc efflux by ZIP13 and its implications for spondylocheiro dysplastic Ehlers–Danlos syndrome
2012
Overview
Significance Intracellular zinc is tightly controlled because zinc is essential but potentially toxic. Many organisms regulate zinc using storage vesicles/organelles, but whether mammals do so is unknown. Here, we show that human ZIP13 releases zinc from vesicular stores. Previous studies found that mutations in the ZIP13 gene, SLC39A13 , cause the spondylocheiro dysplastic form of Ehlers–Danlos syndrome (SCD-EDS) and speculated that ZIP13 exports zinc from the early secretory pathway and that zinc overload in the endoplasmic reticulum causes SCD-EDS. In contrast, our study suggests that SCD-EDS results from zinc deficiency in the endoplasmic reticulum resulting from zinc trapping in vesicular stores.
Publisher
National Academy of Sciences,National Acad Sciences
Subject
/ Cation Transport Proteins - genetics
/ Cation Transport Proteins - physiology
/ Ehlers-Danlos Syndrome - genetics
/ Ehlers-Danlos Syndrome - metabolism
/ Endoplasmic Reticulum - metabolism
/ exports
/ genes
/ Humans
/ Mammals
/ Microscopy, Fluorescence - methods
/ Mutation
/ Proteins
/ RNA, Small Interfering - metabolism
/ toxicity
/ trapping
/ Zinc
