Kv1.1 K+ channels mediate the voltage-dependent potassium ion permeability of excitable membranes and are uniformly distributed in the heart and brain. Kv1.1 play diverse functional roles in several neuronal compartments, especially in the regulation of pre- and post-synaptic membrane excitability. Kv1.2 subunits can co-localize with other Kv1 subunits. For example, Kv1.2 colocalizes with Kv1.1 in the nodes of Ranvier in myelinated axons, and in the brain.
Changes in K+ channel function have been associated with cardiac hypertrophy and failure, apoptosis and oncogenesis, and various neurodegenerative and neuromuscular disorders. Defects in KCNA1 are the cause of episodic ataxia type 1 (EA1) [MIM:160120]; also known as paroxysmal or episodic ataxia with myokymia (EAM) or paroxysmal ataxia with neuromyotonia. EA1 is an autosomal dominant disorder characterized by brief episodes of ataxia and dysarthria. Neurological examination during and between the attacks demonstrates spontaneous, repetitive discharges in the distal musculature (myokymia) that arise from peripheral nerve. Nystagmus is absent
Note: Antibody has been developed by UC Davis under a grant by NIH.
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