作者: Eiichiro Nagata , Hongbo R. Luo , Adolfo Saiardi , Byoung-Il Bae , Norihiro Suzuki
关键词: Inositol Hexakisphosphate Kinase 1 、 Kinase activity 、 Cell biology 、 Cell 、 Inositol hexakisphosphate kinase 2 、 Biochemistry 、 Biology 、 Kinase 、 Apoptosis 、 Programmed cell death 、 Intracellular
摘要: Diphosphoinositol pentakisphosphate (InsP7) and bis-diphosphoinositol tetrakisphosphate contain pyrophosphate bonds. InsP7 is formed from inositol hexakisphosphate (InsP6) by a family of three kinases (InsP6K). In this study we establish one the InsP6Ks, InsP6K2, as physiologic mediator cell death. Overexpression wild-type InsP6K2 augments cytotoxic actions multiple stressors in diverse lines, whereas transfection with dominant negative decreases During death, InsP6 kinase activity enhanced, intracellular level augmented. Deletion but not other forms InsP6K diminishes suggesting that major involved Cytotoxicity associated translocation nuclei to mitochondria, localization isoforms enzyme does change. The present provides compelling evidence endogenous generating InsP7, regulation apoptotic process.