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Updated: Jun 24, 2026

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
Published on: April 27, 2018
Tunicamycin desensitizes store-operated Ca2+ entry to ATP and mitochondrial potential
Aneta Czyź1, Wojciech Brutkowski, Jan Fronk
1The Nencki Institute of Experimental Biology, 3 Pasteur Street, 02-093 Warsaw, Poland.
Abstract:
Tunicamycin effect on thapsigargin-induced store-operated calcium entry was investigated. Ca2+ influx was stimulated by 50% upon exposure of Jurkat cells to tunicamycin. Moreover, tunicamycin efficiently prevented the inhibition of store-operated calcium entry caused by dissipation of mitochondrial membrane potential. Protective action of tunicamycin on store-operated Ca2+ entry was also partially preserved in Jurkat cells depleted of ATP, while Ca2+ entry into ATP-deprived cells grown in tunicamycin-free medium was almost completely inhibited. Tunicamycin-evoked changes in cellular Ca2+ fluxes coincided with decreased glycosylation of STIM1 protein. Although the latter observation is correlative and needs additional confirmation it may suggest that deglycosylation of STIM1 protein deprives store-operated calcium entry system of an important regulatory mechanism. This study suggests a novel mechanism of modulation of the activity of store-operated calcium channels in lymphoidal cells.
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