Episodic ataxia results from voltage-dependent potassium channels with altered functions (Q24312207)

potassium ion transmembrane transporter activity

GOA release 2020-03-11

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A dominantly inherited syndrome with continuous motor neuron discharges.

GOA release 2020-03-11

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M Pessia

3

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author name string

J P Adelman

series ordinal

1

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C T Bond

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2

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J Maylie

series ordinal

4

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language of work or name

English

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publication date

December 1995

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published in

Neuron

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volume

15

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issue

6

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page(s)

1449-54

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cites work

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Autosomal dominant episodic ataxia: a heterogeneous syndrome

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Calcium-activated potassium channels expressed from cloned complementary DNAs

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The S4-S5 loop contributes to the ion-selective pore of potassium channels

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Deletion analysis of K+ channel assembly

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The internal quaternary ammonium receptor site of Shaker potassium channels

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Truncated K+ channel DNA sequences specifically suppress lymphocyte K+ channel gene expression

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Familial periodic ataxia responsive to acetazolamide

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Putative receptor for the cytoplasmic inactivation gate in the Shaker K+ channel

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Evidence that the S6 segment of the Shaker voltage-gated K+ channel comprises part of the pore

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7 January 2021

Episodic ataxia/myokymia syndrome is associated with point mutations in the human potassium channel gene, KCNA1

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Familial paroxysmal kinesigenic ataxia and continuous myokymia

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Identification of two new KCNA1 mutations in episodic ataxia/myokymia families

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The syndrome of continuous muscle fiber activity. Evidence to suggest proximal neurogenic causation

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Acetazolamide-responsive episodic ataxia syndrome

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