Pathophysiological studies of aging Slc39a14 knockout mice to assess the progression of manganese-induced dystonia-parkinsonism
Author:
Publisher
Elsevier BV
Subject
Toxicology,General Neuroscience
Reference51 articles.
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4. Metal transporter Zip14 (Slc39a14) deletion in mice increases manganese deposition and produces neurotoxic signatures and diminished motor activity;Aydemir;J. Neurosci.,2017
5. Intestine-specific deletion of metal transporter Zip14 (Slc39a14) causes brain manganese overload and locomotor defects of manganism;Aydemir;Am. J. Physiol. Gastrointest. Liver Physiol.,2020
Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献
1. Manganese Overexposure Alters Neurogranin Expression and Causes Behavioral Deficits in Larval Zebrafish;International Journal of Molecular Sciences;2024-04-30
2. Physiology of Dystonia: Animal Studies;International Review of Neurobiology;2023
3. Hereditary Disorders of Manganese Metabolism: Pathophysiology of Childhood-Onset Dystonia-Parkinsonism in SLC39A14 Mutation Carriers and Genetic Animal Models;International Journal of Molecular Sciences;2022-10-24
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