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

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Abstract

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by expansion of polyglutamine at 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 abnormal store-dependent response, probably generated by the channels incorporating TRPC1 ( transient receptor potential canonical 1) subunit.

Original languageEnglish (US)
Pages (from-to)206-214
Number of pages9
JournalBiochemistry (Moscow) Supplement Series A: Membrane and Cell Biology
Volume6
Issue number2
DOIs
StatePublished - Apr 1 2012

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Keywords

  • Calcium
  • Huntington's disease
  • Neurodegeneration
  • SOC
  • TRPC1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology

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