Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease

Autores
Wu, Jun; Ryskamp, Daniel; Birnbaumer, Lutz; Bezprozvanny, Ilya
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión aceptada
Descripción
Fil: Wu, Jun. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Ryskamp, Daniel. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Research Triangle Park. Neurobiology Laboratory; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bezprozvanny, Ilya. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Bezprozvanny, Ilya. Peter the Great Saint Petersburg Polytechnic University. Laboratory of Molecular Neurodegeneration; Rusia
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.
Fuente
Journal of Huntington's Disease. 2018;7(1):35–50
Materia
ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/8701
Acceder
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oai_identifier_str oai:ucacris:123456789/8701
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's diseaseWu, JunRyskamp, DanielBirnbaumer, LutzBezprozvanny, IlyaENFERMEDAD DE HUNTINGTONCALCIOTRATAMIENTO MEDICOPROTEINASLUZFil: Wu, Jun. University of Texas. Southwestern Medical Center. Department of Physiology; Estados UnidosFil: Ryskamp, Daniel. University of Texas. Southwestern Medical Center. Department of Physiology; Estados UnidosFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Research Triangle Park. Neurobiology Laboratory; Estados UnidosFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; ArgentinaFil: Bezprozvanny, Ilya. University of Texas. Southwestern Medical Center. Department of Physiology; Estados UnidosFil: Bezprozvanny, Ilya. Peter the Great Saint Petersburg Polytechnic University. Laboratory of Molecular Neurodegeneration; RusiaAbstract: 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.IOS Press2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/87011879-63971879-6400 (online)10.3233/JHD-17026629480205Wu 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/123456789/8701Journal of Huntington's Disease. 2018;7(1):35–50reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:56:54Zoai:ucacris:123456789/8701instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:56:55.052Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
title Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
spellingShingle Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
Wu, Jun
ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
title_short Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
title_full Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
title_fullStr Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
title_full_unstemmed Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
title_sort Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
dc.creator.none.fl_str_mv Wu, Jun
Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
author Wu, Jun
author_facet Wu, Jun
Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
author_role author
author2 Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
author2_role author
author
author
dc.subject.none.fl_str_mv ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
topic ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
dc.description.none.fl_txt_mv Fil: Wu, Jun. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Ryskamp, Daniel. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Research Triangle Park. Neurobiology Laboratory; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bezprozvanny, Ilya. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
Fil: Bezprozvanny, Ilya. Peter the Great Saint Petersburg Polytechnic University. Laboratory of Molecular Neurodegeneration; Rusia
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.
description Fil: Wu, Jun. University of Texas. Southwestern Medical Center. Department of Physiology; Estados Unidos
publishDate 2018
dc.date.none.fl_str_mv 2018
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://repositorio.uca.edu.ar/handle/123456789/8701
1879-6397
1879-6400 (online)
10.3233/JHD-170266
29480205
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
url https://repositorio.uca.edu.ar/handle/123456789/8701
identifier_str_mv 1879-6397
1879-6400 (online)
10.3233/JHD-170266
29480205
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
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv IOS Press
publisher.none.fl_str_mv IOS Press
dc.source.none.fl_str_mv Journal of Huntington's Disease. 2018;7(1):35–50
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
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score 13.22299

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