4.8 Article

BAG-1 induces autophagy for cardiac cell survival

期刊

AUTOPHAGY
卷 5, 期 1, 页码 120-121

出版社

TAYLOR & FRANCIS INC
DOI: 10.4161/auto.5.1.7303

关键词

BAG-1; autophagy; cell survival; protein degradation; cardiac adaptation; heat shock protein; LC3

资金

  1. NIH [HL22559, HL33889, HL34360]
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL033889, R01HL034360, R01HL022559] Funding Source: NIH RePORTER

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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.

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