title: BAG-1 induces autophagy for cardiac cell survival.
abstract: The Bcl-2 associated athanogene (BAG) family of proteins function as cochaperones by bridging molecules that recruit molecular chaperones to target proteins. BAG-1 provides a physical link between the heat shock proteins Hsc70/Hsp70 and the proteasome to facilitate ubiquitin-proteasome-mediated protein degradation. In addition to the proteasome, protein degradation via autophagy is responsible for maintaining cellular metabolism, organelle homeostasis and redox equilibrium. Our recent report shows that autophagy plays an important role in cardiac adaptation-induced cell survival against ischemia-reperfusion injury in association with the BAG-1 protein. BAG-1 is associated with the autophagosomal membrane protein LC3-II and it may participate in the induction of autophagy via Hsc70. Moreover, another BAG family member, BAG-3, is responsible for the induction of macroautophagy in association with HspB8. These results show the involvement of BAG family members in the induction of autophagy for the degradation of damaged or oxidized proteins to promote cell survival.
authors.affiliation: Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA.
authors.forename: Narasimman
authors.initials: N
authors.lastname: Gurusamy
authors.forename: Istvan
authors.initials: I
authors.lastname: Lekli
authors.forename: Mihaela
authors.initials: M
authors.lastname: Gherghiceanu
authors.forename: Lawrence M
authors.initials: LM
authors.lastname: Popescu
authors.forename: Dipak K
authors.initials: DK
authors.lastname: Das
mesh_terms: D000818:Animals; D001343:Autophagy; D002470:Cell Survival; D004268:DNA-Binding Proteins / Q000378:metabolism*; D008954:Models, Biological; D009206:Myocardium / Q000166:cytology; D032383:Myocytes, Cardiac / Q000166:cytology*; D051381:Rats; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: C091732:BCL2-associated athanogene 1 protein; D004268:DNA-Binding Proteins; D014157:Transcription Factors