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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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A Stress-Responsive System for Mitochondrial Protein Degradation

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.
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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.

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

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.
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Pathogenesis of Human Mitochondrial Diseases Is Modulated by Reduced Activity of the Ubiquitin/Proteasome System

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.