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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Tallennettuna:
Bibliografiset tiedot
Julkaisussa:Front Physiol
Päätekijät: Vigont, Vladimir, Kolobkova, Yulia, Skopin, Anton, Zimina, Olga, Zenin, Valery, Glushankova, Lyuba, Kaznacheyeva, Elena
Aineistotyyppi: Artigo
Kieli:Inglês
Julkaistu: Frontiers Media S.A. 2015
Aiheet:
Physiology
Linkit: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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