• A novel KCND3 variant in the N-terminus impairs the ionic current of Kv4.3 and is associated with SCA19/22
• Analysis of SCA8, SCA10, SCA12, SCA17 and SCA19 in patients with unknown spinocerebellar ataxia: a Thai multicentre study
• Expanding the phenotype of SCA19/22: Parkinsonism, cognitive impairment and epilepsy
• First patho-anatomical investigation of the brain of a SCA19 patient
• Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19
• Novel De Novo KCND3 Mutation in a Japanese Patient with Intellectual Disability, Cerebellar Ataxia, Myoclonus, and Dystonia
• Novel Features and Abnormal Pattern of Cerebral Glucose Metabolism in Spinocerebellar Ataxia 19
• Novel SCA19/22-associated KCND3 mutations disrupt human K_V 4.3 protein biosynthesis and channel gating
• Parkinsonism in SCA19/22: Dopamine Transporter Imaging in an Italian Family Harboring a Novel Mutation
• Potential Benefit of Channel Activators in Loss-of-Function Primary Potassium Channelopathies Causing Heredoataxia
• Rare KCND3 Loss-of-Function Mutation Associated With the SCA19/22
• Relationship between type 1 metabotropic glutamate receptors and cerebellar ataxia
• Repolarization matters: mutations in the Kv4.3 potassium channel cause SCA19/22
• Spinocerebellar ataxia type 19/22 mutations alter heterocomplex Kv4.3 channel function and gating in a dominant manner
• The Phenotypic Spectrum of Spinocerebellar Ataxia Type 19 in a Series of Latin American Patients