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Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.contributor.author | Wu, Jun | es |
dc.contributor.author | Ryskamp, Daniel | es |
dc.contributor.author | Birnbaumer, Lutz | es |
dc.contributor.author | Bezprozvanny, Ilya | es |
dc.date.accessioned | 2019-09-09T19:01:05Z | - |
dc.date.available | 2019-09-09T19:01:05Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | 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 | es |
dc.identifier.issn | 1879-6397 | - |
dc.identifier.issn | 1879-6400 (online) | - |
dc.identifier.uri | https://repositorio.uca.edu.ar/handle/123456789/8701 | - |
dc.description.abstract | 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. | es |
dc.format | application/pdf | - |
dc.language.iso | eng | es |
dc.publisher | IOS Press | es |
dc.rights | Acceso Abierto | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.source | Journal of Huntington's Disease. 2018;7(1):35–50 | es |
dc.subject | ENFERMEDAD DE HUNTINGTON | es |
dc.subject | CALCIO | es |
dc.subject | TRATAMIENTO MEDICO | es |
dc.subject | PROTEINAS | es |
dc.subject | LUZ | es |
dc.title | Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease | es |
dc.type | Artículo | es |
dc.identifier.doi | 10.3233/JHD-170266 | - |
dc.identifier.pmid | 29480205 | - |
uca.disciplina | MEDICINA | - |
uca.issnrd | 1 | es |
uca.affiliation | Fil: Wu, Jun. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos | es |
uca.affiliation | Fil: Ryskamp, Daniel. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos | es |
uca.affiliation | Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Research Triangle Park. Neurobiology Laboratory; Estados Unidos | es |
uca.affiliation | Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina | es |
uca.affiliation | Fil: Bezprozvanny, Ilya. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos | es |
uca.affiliation | Fil: Bezprozvanny, Ilya. Peter the Great Saint Petersburg Polytechnic University. Laboratory of Molecular Neurodegeneration; Rusia | es |
uca.version | acceptedVersion | es |
item.grantfulltext | open | - |
item.fulltext | With Fulltext | - |
item.languageiso639-1 | en | - |
crisitem.author.dept | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.dept | Laboratorio de Función y Farmacología de Canales Iónicos | - |
crisitem.author.dept | Consejo Nacional de Investigaciones Científicas y Técnicas | - |
crisitem.author.dept | Facultad de Ciencias Médicas | - |
crisitem.author.orcid | 0000-0002-0775-8661 | - |
crisitem.author.parentorg | Facultad de Ciencias Médicas | - |
crisitem.author.parentorg | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.parentorg | Pontificia Universidad Católica Argentina | - |
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