Modeling Suggests TRPC3 Hydrogen Bonding and Not Phosphorylation Contributes to the Ataxia Phenotype of the Moonwalker Mouse.

Hanson, Sonya M; Sansom, Mark S P; Becker, Esther B E

Hanson, Sonya M; Sansom, Mark S P; Becker, Esther B E.

Affiliation

Hanson SM; Molecular Physiology and Biophysics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, United States.
Sansom MS; Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, United Kingdom.
Becker EB; Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, United Kingdom.

Biochemistry ; 54(26): 4033-41, 2015 Jul 07.

Article in En | MEDLINE | ID: mdl-26112884

Subject(s)

Cerebellar Ataxia/genetics; Point Mutation; TRPC Cation Channels/genetics; TRPC Cation Channels/metabolism; Amino Acid Sequence; Animals; Calcium/metabolism; Cell Line; Cerebellar Ataxia/metabolism; Cerebellar Ataxia/pathology; Hydrogen Bonding; Mice; Models, Molecular; Molecular Sequence Data; Neurons/metabolism; Neurons/pathology; Phenotype; Phosphorylation; Sequence Alignment; TRPC Cation Channels/analysis

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Full text: 1 Database: MEDLINE Main subject: Cerebellar Ataxia / Point Mutation / TRPC Cation Channels Type of study: Prognostic_studies Limits: Animals Language: En Journal: Biochemistry Year: 2015 Type: Article Affiliation country: United States

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