![]() Indeed, MCL1 overexpression is sufficient to inhibit recruitment to mitochondria of the E3 Ubiquitin ligase HUWE1, a crucial dynamic partner of AMBRA1, upon AMBRA1-mediated mitophagy induction. ![]() Here, we investigated the role of BCL2-family proteins on AMBRA1-dependent mitophagy and showed that MCL1 delays AMBRA1-dependent mitophagy. A critical unresolved issue is how AMBRA1-mediated mitophagy is controlled in response to cellular stress. AMBRA1 is a mitophagy receptor for the selective removal of damaged mitochondria in mammalian cells. mitophagy is a crucial process involved in mitochondria quality control. 11 Department of Pediatric Hematology and Oncology, IRCCS Bambino Gesù Children's Hospital, Rome, Italy. 10 Unit of Cell Stress and Survival, Center for Autophagy, Recycling and Disease (CARD), Danish Cancer Society Research Center, 2100, Copenhagen, Denmark. 9 Department of Biology, University of Rome Tor Vergata, 00133, Rome, Italy.8 MRC Toxicology Unit, University of Cambridge, Cambridge, UK.7 Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy.6 Department of Gynecology/Obstetrics and Pediatrics, Sapienza University, Rome, Italy.5 Department of Paediatric Oncohematology and Cell and Gene therapy, IRCCS Ospedale pediatrico Bambino Gesù, 00143, Rome, Italy.4 National Research Council of Italy (CNR) Institute of Translational Pharmacology IFT Via Fosso del Cavaliere 100, 00133, Rome, Italy.3 Department of Biology, University of Rome Tor Vergata, 00133, Rome, Italy.2 IRCCS Fondazione Santa Lucia, 00143, Rome, Italy. 1 IRCCS Fondazione Santa Lucia, 00143, Rome, Italy.
0 Comments
Leave a Reply. |