Copper – a novel stimulator of autophagy

Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang et al. (Nat Cell Biol, doi: 10.1038/s41556-020-0481-4) demonstrate that copper binds with high affinity to a designated interaction site in the pro-...

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Main Authors: Hans Zischka, Guido Kroemer
Format: Article
Language:English
Published: Shared Science Publishers OG 2020-04-01
Series:Cell Stress
Subjects:
Online Access:http://www.cell-stress.com/researcharticles/2020a-zischka-cell-stress/
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author Hans Zischka
Guido Kroemer
author_facet Hans Zischka
Guido Kroemer
author_sort Hans Zischka
collection DOAJ
description Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang et al. (Nat Cell Biol, doi: 10.1038/s41556-020-0481-4) demonstrate that copper binds with high affinity to a designated interaction site in the pro-autophagic kinases ULK1 and ULK2. Chelation of copper or genetic deletion of this copper-binding site inhibits autophagy and hence reduces the fitness of KRAS-induced cancers. These findings suggest that copper chelation might constitute a novel therapeutic intervention on autophagy-dependent malignancies.
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spelling doaj.art-c181b74508244a7d8da569a4e5426fc82022-12-21T23:45:55ZengShared Science Publishers OGCell Stress2523-02042020-04-0145929410.15698/cst2020.05.218Copper – a novel stimulator of autophagyHans Zischka0Guido Kroemer1Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany.Centre de Recherche des Cordeliers, Equipe labellisée par la Ligue contre le cancer, Université de Paris, Sorbonne Université, IN-SERM U1138, Institut Universitaire de France, Paris, France.Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang et al. (Nat Cell Biol, doi: 10.1038/s41556-020-0481-4) demonstrate that copper binds with high affinity to a designated interaction site in the pro-autophagic kinases ULK1 and ULK2. Chelation of copper or genetic deletion of this copper-binding site inhibits autophagy and hence reduces the fitness of KRAS-induced cancers. These findings suggest that copper chelation might constitute a novel therapeutic intervention on autophagy-dependent malignancies.http://www.cell-stress.com/researcharticles/2020a-zischka-cell-stress/autophagywilson diseasecoppercancerulk1ulk2mek1
spellingShingle Hans Zischka
Guido Kroemer
Copper – a novel stimulator of autophagy
Cell Stress
autophagy
wilson disease
copper
cancer
ulk1
ulk2
mek1
title Copper – a novel stimulator of autophagy
title_full Copper – a novel stimulator of autophagy
title_fullStr Copper – a novel stimulator of autophagy
title_full_unstemmed Copper – a novel stimulator of autophagy
title_short Copper – a novel stimulator of autophagy
title_sort copper a novel stimulator of autophagy
topic autophagy
wilson disease
copper
cancer
ulk1
ulk2
mek1
url http://www.cell-stress.com/researcharticles/2020a-zischka-cell-stress/
work_keys_str_mv AT hanszischka copperanovelstimulatorofautophagy
AT guidokroemer copperanovelstimulatorofautophagy