There is general agreement in the literature that Ca2+ efflux from the ER and Ca2+ accumulation into the mitochondria are linked to the effects of various apoptotic stimuli [18].
The task of this work was to evaluate the effect of the overexpression of a constitutively active AKT1 on subcellular Ca2+ Ruxolitinib in transiently transfected HeLa cells, i.e. the same cell model in which the effects of Bcl-2 and Bax on Ca2+ signaling were previously detected and analyzed [19], [20] and [21]. We then analyzed the effects of Akt overexpression on the cytosolic Ca2+ signal elicited by apoptotic stimuli such as oxidative stress and arachidonic acid, as digestion act through mitochondrial Ca2+ overload and activation of the intrinsic apoptotic pathway following to Ca2+ release from the ER.
Altogether our data suggest that the alteration of Ca2+ fluxes through the IP3R is a key component of the protective action of Akt against apoptosis induced by stimuli acting in a Ca2+-sensitive manner.
Materials and methods
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