Protein mutated in paroxysmal dyskinesia interacts with the active zone protein RIM and suppresses synaptic vesicle exocytosis
Copyright policy )Protein mutated in paroxysmal dyskinesia interacts with the active zone protein RIM and suppresses synaptic vesicle exocytosis
Significance Paroxysmal nonkinesigenic dyskinesia (PNKD) is an autosomal dominant episodic movement disorder precipitated by coffee, alcohol, and stress. Here, we show that PNKD interacts with synaptic active zone proteins Rab3-interacting molecule (RIM)1 and RIM2, localizes to synapses, and modulates neurotransmitter release. PNKD knockout mice have impaired synaptic transmission and short-term plasticity.
- University of California, San Francisco United States
- Stanford University United States
- Howard Hughes Medical Institute United States
- Excellence Cluster Universe Germany
Mice, Knockout, paroxysmal dyskinesia, Knockout, 1.1 Normal biological development and functioning, Neurosciences, Muscle Proteins, Exocytosis, Brain Disorders, Mice, Underpinning research, Chorea, Animals, ATP-Binding Cassette Transporters, Synaptic Vesicles, neurological disease, exocytosis, Protein Binding
Mice, Knockout, paroxysmal dyskinesia, Knockout, 1.1 Normal biological development and functioning, Neurosciences, Muscle Proteins, Exocytosis, Brain Disorders, Mice, Underpinning research, Chorea, Animals, ATP-Binding Cassette Transporters, Synaptic Vesicles, neurological disease, exocytosis, Protein Binding
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