STIM1 Protein Activates Store-Operated Calcium Channels in Cellular Model of Huntington’s Disease

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Abstract


We have shown that the expression of full-length mutated huntingtin in human neuroblastoma cells (SK-N-SH) leads to an abnormal increase in calcium entry through store-operated channels. In this paper, the expression of the N-terminal fragment of mutated huntingtin (Htt138Q-1exon) is shown to be enough to provide an actual model for Huntington’s disease. We have shown that Htt138Q-1exon expression causes increased store-operated calcium entry, which is mediated by at least two types of channels in SK-N-SH cells with different reversal potentials. Calcium sensor, STIM1, is required for activation of store-operated calcium entry in these cells. The results provide grounds for considering the proteins responsible for the activation and maintenance of the store-operated calcium entry as promising targets for developing novel therapeutics for neurodegenerative diseases.


V. A. Vigont

Institute of Cytology, Russian Academy of Sciences

Author for correspondence.
Email: evkazn@incras.ru

Russian Federation

O. A. Zimina

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

L. N. Glushankova

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

J. A. Kolobkova

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

M. A. Ryazantseva

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

G. N. Mozhayeva

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

E. V. Kaznacheyeva

Institute of Cytology, Russian Academy of Sciences

Email: evkazn@incras.ru

Russian Federation

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Copyright (c) 2014 Vigont V.A., Zimina O.A., Glushankova L.N., Kolobkova J.A., Ryazantseva M.A., Mozhayeva G.N., Kaznacheyeva E.V.

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