Commentary to: “The Pathophysiology and Clinical Manifestations of Spinocerebellar Ataxia Type 6” by Rentiya et al., Cerebellum 2020;19(3):459–464)
Author:
Publisher
Springer Science and Business Media LLC
Subject
Clinical Neurology,Neurology
Link
https://link.springer.com/content/pdf/10.1007/s12311-020-01221-8.pdf
Reference10 articles.
1. Tsunemi T, Ishikawa K, Jin H, Mizusawa H. Cell-type-specific alternative splicing in spinocerebellar ataxia type 6. Neurosci Lett. 2008;47:78–81.
2. Watase K, Barrett CF, Miyazaki T, Ishiguro T, Ishikawa K, Hu Y, et al. Spinocerebellar ataxia type 6 knockin mice develop a progressive neuronal dysfunction with age-dependent accumulation of mutant CaV2.1 channels. Proc Natl Acad Sci U S A. 2008;105:11987–92.
3. Tsou W-L, Soong B-W, Paulson HL, Rodríguez-Lebrón E. Splice isoform-specific suppression of the CaV2.1 variant underlying spinocerebellar ataxia type 6. Neurobiol Dis. 2011;43:533–42.
4. Du X, Wang J, Zhu H, Rinaldo L, Lamar KM, Palmenberg AC, et al. Second cistron in CACNA1A gene encodes a transcription factor mediating cerebellar development and SCA6. Cell. 2013;154:118–33.
5. Zhuchenko O, Bailey J, Bonnen P, Ashizawa T, Stockton DW, Amos C, et al. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha1A-voltage-dependent calcium channel. Nat Genet. 1997;15(1):62–9.
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