caa a22 4500 44582476X CHVBK 20180317145255.0 cr unu---uuuuu 170323e20110301xx s 000 0 eng 10.1007/s00246-010-9879-2 doi (NATIONALLICENCE)springer-10.1007/s00246-010-9879-2 Muslin Anthony Center for Cardiovascular Research, Washington University School of Medicine, 660 South Euclid Avenue, Box 8086, 63110, St. Louis, MO, USA aut Akt2: A Critical Regulator of Cardiomyocyte Survival and Metabolism [Elektronische Daten] [Anthony Muslin] Akt proteins are serine/threonine protein kinases that participate in several important intracellular signal transduction cascades. Akt1 and Akt2 are expressed in cardiomyocytes, and both are activated by the action of a variety of growth factors and extracellular ligands. In work with genetically modified mice that had targeted disruption of the genes encoding Akt1 or Akt2, findings showed that Akt1 specifically regulated the physiologic growth of cardiomyocytes that occurred in response to exercise training. In contrast, Akt2 does not regulate physiologic growth but instead regulates glucose metabolism in response to insulin stimulation in cardiomyocytes. Furthermore, Akt2 plays a critical role in antagonizing cardiomyocyte apoptosis that occurs in response to a variety of stimuli, including pathologic remodeling after experimental myocardial infarction. In addition, the protein tribbles 3 (TRB3), an Akt antagonist, was found to be expressed in cardiomyocytes and to be induced by stimuli that cause endoplasmic reticulum stress. Endoplasmic reticulum stress-mediated antagonism of Akt signaling in cardiomyocytes was dependent on TRB3 induction. Finally, myocardial infarction caused endoplasmic reticulum stress in the infarct border zone that was associated with TRB3 induction. These results demonstrate the differential roles of Akt family members and the importance of Akt2 in cardiomyocyte survival. Springer Science+Business Media, LLC, 2011 Akt proteins nationallicence Cardiomyocyte survival nationallicence Endoplasmic reticulum stress nationallicence Pediatric Cardiology Springer-Verlag 32/3(2011-03-01), 317-322 0172-0643 32:3<317 2011 32 246 https://doi.org/10.1007/s00246-010-9879-2 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00246-010-9879-2 text/html Onlinezugriff via DOI NATIONALLICENCE 100 1- Muslin Anthony Center for Cardiovascular Research, Washington University School of Medicine, 660 South Euclid Avenue, Box 8086, 63110, St. Louis, MO, USA aut NATIONALLICENCE 773 0- Pediatric Cardiology Springer-Verlag 32/3(2011-03-01), 317-322 0172-0643 32:3<317 2011 32 246 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer