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Tunicamycin desensitizes store-operated Ca2+ entry to ATP and mitochondrial potential.

Authors :
Czyź A
Brutkowski W
Fronk J
Duszyński J
Zabłocki K
Source :
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2009 Apr 03; Vol. 381 (2), pp. 176-80. Date of Electronic Publication: 2009 Feb 11.
Publication Year :
2009

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.

Details

Language :
English
ISSN :
1090-2104
Volume :
381
Issue :
2
Database :
MEDLINE
Journal :
Biochemical and biophysical research communications
Publication Type :
Academic Journal
Accession number :
19338771
Full Text :
https://doi.org/10.1016/j.bbrc.2009.02.006