title: Tunicamycin desensitizes store-operated Ca2+ entry to ATP and mitochondrial potential.
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.
authors.affiliation: The Nencki Institute of Experimental Biology, 3 Pasteur Street, 02-093 Warsaw, Poland.
authors.forename: Aneta
authors.initials: A
authors.lastname: Czyź
authors.forename: Wojciech
authors.initials: W
authors.lastname: Brutkowski
authors.forename: Jan
authors.initials: J
authors.lastname: Fronk
authors.forename: Jerzy
authors.initials: J
authors.lastname: Duszyński
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Zabłocki