Store-operated calcium entry into SK-N-SH human neuroblastoma cells modeling Huntington's disease

V. A. Vigont, O. A. Zimina, L. N. Glushankova, I. B. Bezprozvanny, G. N. Mozhayeva, E. V. Kaznacheyeva

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by expansion of polyglutamine on the N-terminus of the huntingtin protein. Striatal medium spiny neurons (MSN) are the primary targets of HD pathology. In our study, a cellular model of HD was based on the human neuroblastoma cells SK-N-SH transfected with plasmid for expression of the mutant huntingtin protein Htt138Q. Expression of Htt138Q increased store-dependent calcium entry into SK-N-SH cells. EVP4593 reversibly blocked the anomalous store-dependent response, probably generated by the channels incorporating TRPC1 (short transient receptor potential channel 1) subunit.

Original languageEnglish (US)
Pages (from-to)123-132
Number of pages10
JournalBiologicheskie Membrany
Volume29
Issue number1-2
StatePublished - Dec 3 2012

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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    Vigont, V. A., Zimina, O. A., Glushankova, L. N., Bezprozvanny, I. B., Mozhayeva, G. N., & Kaznacheyeva, E. V. (2012). Store-operated calcium entry into SK-N-SH human neuroblastoma cells modeling Huntington's disease. Biologicheskie Membrany, 29(1-2), 123-132.