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Tunicamycin desensitizes store-operated Ca2+ entry to ATP and mitochondrial potential.
- 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.
- Subjects :
- Calcium Signaling drug effects
Glycosylation
Humans
Jurkat Cells
ORAI1 Protein
Stromal Interaction Molecule 1
Thapsigargin antagonists & inhibitors
Thapsigargin pharmacology
Adenosine Triphosphate metabolism
Calcium metabolism
Calcium Channels metabolism
Membrane Potential, Mitochondrial drug effects
Membrane Proteins metabolism
Neoplasm Proteins metabolism
Tunicamycin pharmacology
Subjects
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