Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8701
Título : Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
Autor : Wu, Jun 
Ryskamp, Daniel 
Birnbaumer, Lutz 
Bezprozvanny, Ilya 
Palabras clave : ENFERMEDAD DE HUNTINGTONCALCIOTRATAMIENTO MEDICOPROTEINASLUZ
Fecha de publicación : 2018
Editorial : IOS Press
Cita : Wu J, Ryskamp D, Birnbaumer L, Bezprozvanny I. Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease [en línea]. Journal of Huntington's Disease. 2018;7(1):35–50. doi:10.3233/JHD-170266 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8701
Resumen : Abstract: Huntington disease (HD) is a dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. We previously discovered that mutant Huntingtin sensitizes type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) to InsP3. This causes calcium leakage from the endoplasmic reticulum (ER) and a compensatory increase in neuronal store-operated calcium (nSOC) entry. We previously demonstrated that supranormal nSOC leads to synaptic loss in striatal medium spiny neurons (MSNs) in YAC128 HD mice.
URI : https://repositorio.uca.edu.ar/handle/123456789/8701
ISSN : 1879-6397
1879-6400 (online)
Disciplina: MEDICINA
DOI: 10.3233/JHD-170266
Derechos: Acceso Abierto
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