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

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...

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Detalles Bibliográficos
Autores principales: Wu, Jun, Ryskamp, Daniel, Birnbaumer, Lutz, Bezprozvanny, Ilya
Formato: Artículo
Lenguaje:Inglés
Publicado: IOS Press 2019
Materias:
ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/8701
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139123456789-8701
record_format dspace
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
spellingShingle ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
Wu, Jun
Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
topic_facet ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
description 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.
format Artículo
author Wu, Jun
Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
author_facet Wu, Jun
Ryskamp, Daniel
Birnbaumer, Lutz
Bezprozvanny, Ilya
author_sort Wu, Jun
title Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease
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
publisher IOS Press
publishDate 2019
url https://repositorio.uca.edu.ar/handle/123456789/8701
work_keys_str_mv AT wujun inhibitionoftrpc1dependentstoreoperatedcalciumentryimprovessynapticstabilityandmotorperformanceinamousemodelofhuntingtonsdisease
AT ryskampdaniel inhibitionoftrpc1dependentstoreoperatedcalciumentryimprovessynapticstabilityandmotorperformanceinamousemodelofhuntingtonsdisease
AT birnbaumerlutz inhibitionoftrpc1dependentstoreoperatedcalciumentryimprovessynapticstabilityandmotorperformanceinamousemodelofhuntingtonsdisease
AT bezprozvannyilya inhibitionoftrpc1dependentstoreoperatedcalciumentryimprovessynapticstabilityandmotorperformanceinamousemodelofhuntingtonsdisease
bdutipo_str Repositorios
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