title: AMPK, MAPK and Bax in the heart: some questions answered.
abstract: The question of how Bax is activated during apoptosis to perform its role in permeabilization of mitochondrial membranes is intriguing for investigators in the wide field of cell death research. In their paper published in the Biochemical Journal in 2006, Capano and Crompton presented their discovery that simulated ischaemia causes rapid activation of AMPK (AMP-activated protein kinase) which phosphorylates and activates p38 MAPK (mitogen-activated protein kinase) leading to Bax activation and translocation to mitochondria in isolated cardiac myocytes. This was the first report on the molecular mechanism of Bax activation and migration during ischaemia-induced apoptosis in cardiomyocytes.
authors.affiliation: Institute for Biomedical Research, Kaunas University of Medicine, Kaunas, LT 50009, Lithuania. vilbor@vector.kmu.lt
authors.forename: Vilmante
authors.initials: V
authors.lastname: Borutaite
mesh_terms: D000263:Adenylate Kinase / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D004789:Enzyme Activation; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
chemical_list: D051028:bcl-2-Associated X Protein; D020928:Mitogen-Activated Protein Kinases; D000263:Adenylate Kinase