Associated Papers
Activation of a Potassium Channel Mutation That Causes Spinocerebellar Ataxia Promotes Aggregation of the RhoGEF Domain-Containing Protein Plekhg4.
Zhang Y et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2025
A novel KCNC3 gene variant in the voltage-dependent Kv3.3 channel in an atypical form of SCA13 with dominant central vertigo.
Bernhard FP et al.
Frontiers in Cellular Neuroscience, 2024
Multiple Roles of Actin in Exo- and Endocytosis.
Wu LG et al.
Frontiers in Synaptic Neuroscience, 2022
Suppression of Kv3.3 channels by antisense oligonucleotides reverses biochemical effects and motor impairment in spinocerebellar ataxia type 13 mice.
Zhang Y et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2021
Cerebellar Kv3.3 potassium channels activate TANK-binding kinase 1 to regulate trafficking of the cell survival protein Hax-1.
Zhang Y et al.
Nature Communications, 2021
Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesicles.
Wu XS et al.
Neuron, 2021
Neurological Disease Modelling for Spinocerebellar Ataxia Using Zebrafish.
Namikawa K et al.
Journal of Experimental Neuroscience, 2019
C-terminal proline deletions in KCNC3 cause delayed channel inactivation and an adult-onset progressive SCA13 with spasticity.
Khare S et al.
Cerebellum (london, England), 2018
Kv3.3 Channels Bind Hax-1 and Arp2/3 to Assemble a Stable Local Actin Network that Regulates Channel Gating.
Zhang Y et al.
Cell, 2016
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