CaMKII Inhibition Attenuates Distinct Gain-of-Function Effects Produced by Mutant Nav1.6 Channels and Reduces Neuronal Excitability.

Zybura, Agnes S; Sahoo, Firoj K; Hudmon, Andy; Cummins, Theodore R

Zybura, Agnes S; Sahoo, Firoj K; Hudmon, Andy; Cummins, Theodore R.

Afiliación

Zybura AS; Program in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Sahoo FK; Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN 47907, USA.
Hudmon A; Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN 47907, USA.
Cummins TR; Program in Medical Neuroscience, Paul and Carole Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Cells ; 11(13)2022 07 04.

Article en En | MEDLINE | ID: mdl-35805192

Asunto(s)

Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina; Epilepsia; Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina/genética; Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina/metabolismo; Epilepsia/genética; Epilepsia/metabolismo; Mutación con Ganancia de Función; Humanos; Neuronas/metabolismo; Técnicas de Placa-Clamp

Palabras clave

CaMKII; Nav1.6; electrophysiology; phosphorylation; post-translational modification (PTM); sodium channel

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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Epilepsia / Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cells Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos

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