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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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| Publicado no: | Front Physiol |
|---|---|
| Main Authors: | , , , , , , |
| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
Frontiers Media S.A.
2015
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4656824/ https://ncbi.nlm.nih.gov/pubmed/26635623 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3389/fphys.2015.00337 |
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