Abstract
The Golgi apparatus (GA) is a bona fide Ca(2+) store; however, there is a lack of GA-specific Ca(2+) mobilizing agents. Here, we report that emetine specifically releases Ca(2+) from GA in HeLa and HL-1 atrial myocytes. Additionally, it has become evident that the trans-Golgi is a labile Ca(2+) store that requires a continuous source of Ca(2+) from either the external milieu or from the ER, to enable it to produce a detectable transient increase in cytosolic Ca(2+). Our data indicates that the emetine-sensitive Ca(2+) mobilizing mechanism is different from the two classical Ca(2+) release mechanisms, i.e. IP(3) and ryanodine receptors. This newly discovered ability of emetine to release Ca(2+) from the GA may explain why chronic consumption of ipecac syrup has muscle side effects.