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Mutations in SLC39A14 disrupt manganese homeostasis and cause childhood onset parkinsonismdystonia Citation Busch, K., E. Meyer, L. E. Maldivian, N. Zhao, C. Dad swell, A. Abdullah, C. Y. Hung, et
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Mutations in SLC39A14 disrupt the function of the SLC39A14 gene, which is involved in zinc transport in the body, leading to various health issues.
Individuals or institutions conducting genetic research or clinical studies involving SLC39A14 mutations are typically required to file such information.
Filling out mutations in SLC39A14 disrupt involves collecting genetic data, documenting the specific mutations identified, and submitting the findings through the designated reporting channels.
The purpose of reporting mutations in SLC39A14 is to advance understanding of related genetic disorders and to facilitate the development of treatment strategies.
Information that must be reported includes the type of mutation, its effects on gene function, associated health conditions, and demographic data of affected individuals.
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