Human Golgi antiapoptotic protein modulates intracellular calcium fluxes.
SourceMolecular Biology of the Cell, 20, 16, (2009), pp. 3638-45
Article / Letter to editor
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Cell Biology (UMC)
Molecular Biology of the Cell
SubjectIGMD 8: Mitochondrial medicine; N4i 1: Pathogenesis and modulation of inflammation; NCMLS 1: Infection and autoimmunity; NCMLS 4: Energy and redox metabolism; NCMLS 5: Membrane transport and intracellular motility
Golgi antiapoptotic protein (GAAP) is a novel regulator of cell death that is highly conserved in eukaryotes and present in some poxviruses, but its molecular mechanism is unknown. Given that alterations in intracellular Ca(2+) homeostasis play an important role in determining cell sensitivity to apoptosis, we investigated if GAAP affected Ca(2+) signaling. Overexpression of human (h)-GAAP suppressed staurosporine-induced, capacitative Ca(2+) influx from the extracellular space. In addition, it reduced histamine-induced Ca(2+) release from intracellular stores through inositol trisphosphate receptors. h-GAAP not only decreased the magnitude of the histamine-induced Ca(2+) fluxes from stores to cytosol and mitochondrial matrices, but it also reduced the induction and frequency of oscillatory changes in cytosolic Ca(2+). Overexpression of h-GAAP lowered the Ca(2+) content of the intracellular stores and decreased the efficacy of IP(3), providing possible explanations for the observed results. Opposite effects were obtained when h-GAAP was knocked down by siRNA. Thus, our data demonstrate that h-GAAP modulates intracellular Ca(2+) fluxes induced by both physiological and apoptotic stimuli.
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