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Both Orai1 and TRPC1 are Involved in Excessive Store-Operated Calcium Entry in Striatal Neurons Expressing Mutant Huntingtin Exon 1

It has been previously reported that N-terminus of mutant huntingtin (product of the 1st exon) is sufficient to cause a Huntington's disease (HD) pathological phenotype. In view of recent data suggesting that improper regulation of store-operated calcium (SOC) channels is involved in neurodegen...

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Detalles Bibliográficos
Autores principales: Vigont, Vladimir, Kolobkova, Yulia, Skopin, Anton, Zimina, Olga, Zenin, Valery, Glushankova, Lyuba, Kaznacheyeva, Elena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656824/
https://www.ncbi.nlm.nih.gov/pubmed/26635623
http://dx.doi.org/10.3389/fphys.2015.00337

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