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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 HUNTINGTON; CALCIO; TRATAMIENTO MEDICO; PROTEINAS; LUZ | 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 |
| Aparece en las colecciones: | Artículos |
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| inhibition-trpc1-dependent-store.pdf | 1,4 MB | Adobe PDF |  Visualizar/Abrir |
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