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

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 journal › Article › peer-review

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 language	English (US)
Pages (from-to)	123-132
Number of pages	10
Journal	Biologicheskie Membrany
Volume	29
Issue number	1-2
State	Published - Dec 3 2012

ASJC Scopus subject areas

Molecular Biology
Cell Biology

Cite this

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

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.",

author = "Vigont, {V. A.} and Zimina, {O. A.} and Glushankova, {L. N.} and Bezprozvanny, {I. B.} and Mozhayeva, {G. N.} and Kaznacheyeva, {E. V.}",

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AU - Vigont, V. A.

AU - Zimina, O. A.

AU - Glushankova, L. N.

AU - Bezprozvanny, I. B.

AU - Mozhayeva, G. N.

AU - Kaznacheyeva, E. V.

PY - 2012/12/3

Y1 - 2012/12/3

N2 - 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.

AB - 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.

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

Abstract

ASJC Scopus subject areas

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