Both Orai1 and TRPC1 are involved in excessive store-operated calcium entry in striatal neurons expressing mutant huntingtin exon 1

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 neurodegenerati...

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Bibliographic Details
Main Authors: Vladimir eVigont, Juliya eKolobkova, Anton eSkopin, Olga eZimina, Lyuba eGlushankova, Elena eKaznacheyeva
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-11-01
Series:Frontiers in Physiology
Subjects:
neurodegeneration
ionic channels
Huntington’s disease
Orai1
STIM1
store-operated calcium entry
Online Access:http://journal.frontiersin.org/Journal/10.3389/fphys.2015.00337/full

Internet

http://journal.frontiersin.org/Journal/10.3389/fphys.2015.00337/full

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