N
Nurit Livnat-Levanon
Researcher at Technion – Israel Institute of Technology
Publications - 17
Citations - 1256
Nurit Livnat-Levanon is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Proteasome & Mitochondrion. The author has an hindex of 14, co-authored 17 publications receiving 1134 citations.
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Journal ArticleDOI
A Stress-Responsive System for Mitochondrial Protein Degradation
Jin-Mi Heo,Nurit Livnat-Levanon,Eric B. Taylor,Kevin T. Jones,Noah Dephoure,Julia Ring,Jianxin Xie,Jeffrey L. Brodsky,Frank Madeo,Steven P. Gygi,Kaveh Ashrafi,Michael H. Glickman,Jared Rutter +12 more
TL;DR: It is demonstrated that Ydr049 (renamed VCP/Cdc48-associated mitochondrial stress-responsive--Vms1), a member of an unstudied pan-eukaryotic protein family, translocates from the cytosol to mitochondria upon mitochondrial stress.
Journal ArticleDOI
Ubiquitin–Proteasome System and mitochondria — Reciprocity
TL;DR: The regulation of mitochondrial morphology and metabolic function by UPS, as well as the reciprocal relationship between aberrant ROS produced by mitochondria and ubiquitination or proteasome activity are addressed.
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Ubiquitin-proteasome-dependent degradation of a mitofusin, a critical regulator of mitochondrial fusion.
Mickael M. Cohen,Guillaume P. Leboucher,Nurit Livnat-Levanon,Michael H. Glickman,Allan M. Weissman +4 more
TL;DR: This study provides a framework for developing an understanding of the function of Mdm30p-mediated Fzo1p degradation in the multistep process of mitochondrial fusion and provides the first demonstration that a cytosolic ubiquitin ligase targets a critical regulatory molecule at the mitochondrial outer membrane.
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Reversible 26S Proteasome Disassembly upon Mitochondrial Stress
Nurit Livnat-Levanon,Éva Kevei,Oded Kleifeld,Daria Krutauz,Alexandra Segref,Teresa Rinaldi,Zoi Erpapazoglou,Mickael M. Cohen,Noa Reis,Thorsten Hoppe,Michael H. Glickman +10 more
TL;DR: It is shown that acute oxidative stress caused by environmental insults or mitochondrial defects results in rapid disassembly of 26S proteasomes into intact 20S core and 19S regulatory particles, and polyubiquitinated substrates accumulate, mitochondrial networks fragment, and cellular reactive oxygen species (ROS) levels increase.
Journal ArticleDOI
Pathogenesis of Human Mitochondrial Diseases Is Modulated by Reduced Activity of the Ubiquitin/Proteasome System
Alexandra Segref,Éva Kevei,Wojciech Pokrzywa,Kathrin Schmeisser,Johannes Mansfeld,Johannes Mansfeld,Nurit Livnat-Levanon,Regina Ensenauer,Michael H. Glickman,Michael Ristow,Michael Ristow,Thorsten Hoppe +11 more
TL;DR: A link between mitochondrial stress and ubiquitin-dependent proteolysis is identified, which supports cellular surveillance both in Caenorhabditis elegans and humans and provides a valuable target for therapeutic intervention.