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 (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-autopha...

Full description

Saved in:
Bibliographic Details
Published in:Cell Stress 2020-04, Vol.4 (5), p.92-94
Main Authors: Zischka, Hans, Kroemer, Guido
Format: Article
Language:English
Subjects:
and Thoughts
Autophagy
Cancer
Copper
mek1
ulk1
ulk2
Wilson Disease
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c459t-accbf6f26f560b696b9e5e668b0b5e66d314fea4c6f66b35467d777eace1d6663
cites
container_end_page 94
container_issue 5
container_start_page 92
container_title Cell Stress
container_volume 4
creator Zischka, Hans
Kroemer, Guido
description Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang (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.
doi_str_mv 10.15698/cst2020.05.218
format article
fullrecord <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_c181b74508244a7d8da569a4e5426fc8</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_c181b74508244a7d8da569a4e5426fc8</doaj_id><sourcerecordid>2404382358</sourcerecordid><originalsourceid>FETCH-LOGICAL-c459t-accbf6f26f560b696b9e5e668b0b5e66d314fea4c6f66b35467d777eace1d6663</originalsourceid><addsrcrecordid>eNpVkctLw0AQxhdRrGjP3iRHL6n7nGwughRfUPCi52Wy2dSUpBt3k0L_e9OHoqcZ5vH7hvkIuWZ0xhTk-s7GnlNOZ1TNONMn5IIrLtKxIk__5BMyjXFFKeUMdKbgnEwEl5wqnl-Q27nvOheSNMFk7TeuSWJft0ODvQ-JrxIcet994nJ7Rc4qbKKbHuMl-Xh6fJ-_pIu359f5wyK1UuV9itYWFVQcKgW0gByK3CkHoAta7GIpmKwcSgsVQCGUhKzMssyhdawEAHFJXg_c0uPKdKFuMWyNx9rsCz4sDYa-to0zlmlWZFJRzaXErNQljm9B6ZQc9a0eWfcHVjcUrSutW_cBm3_Q_511_WmWfmMyzrgSfATcHgHBfw0u9qato3VNg2vnh2i4pFJoLtRO6-4waoOPMbjqV4ZRs7fLHO0yVJnRrnHj5u91v_M_5ohvSOGPuQ</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2404382358</pqid></control><display><type>article</type><title>Copper - a novel stimulator of autophagy</title><source>Open Access: PubMed Central</source><creator>Zischka, Hans ; Kroemer, Guido</creator><creatorcontrib>Zischka, Hans ; Kroemer, Guido</creatorcontrib><description>Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang (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.</description><identifier>ISSN: 2523-0204</identifier><identifier>EISSN: 2523-0204</identifier><identifier>DOI: 10.15698/cst2020.05.218</identifier><identifier>PMID: 32420529</identifier><language>eng</language><publisher>Austria: Shared Science Publishers OG</publisher><subject>and Thoughts ; Autophagy ; Cancer ; Copper ; mek1 ; ulk1 ; ulk2 ; Wilson Disease</subject><ispartof>Cell Stress, 2020-04, Vol.4 (5), p.92-94</ispartof><rights>Copyright: © 2020 Zischka and Kroemer.</rights><rights>Copyright: © 2020 Zischka and Kroemer 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-accbf6f26f560b696b9e5e668b0b5e66d314fea4c6f66b35467d777eace1d6663</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212532/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212532/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32420529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zischka, Hans</creatorcontrib><creatorcontrib>Kroemer, Guido</creatorcontrib><title>Copper - a novel stimulator of autophagy</title><title>Cell Stress</title><addtitle>Cell Stress</addtitle><description>Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang (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.</description><subject>and Thoughts</subject><subject>Autophagy</subject><subject>Cancer</subject><subject>Copper</subject><subject>mek1</subject><subject>ulk1</subject><subject>ulk2</subject><subject>Wilson Disease</subject><issn>2523-0204</issn><issn>2523-0204</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkctLw0AQxhdRrGjP3iRHL6n7nGwughRfUPCi52Wy2dSUpBt3k0L_e9OHoqcZ5vH7hvkIuWZ0xhTk-s7GnlNOZ1TNONMn5IIrLtKxIk__5BMyjXFFKeUMdKbgnEwEl5wqnl-Q27nvOheSNMFk7TeuSWJft0ODvQ-JrxIcet994nJ7Rc4qbKKbHuMl-Xh6fJ-_pIu359f5wyK1UuV9itYWFVQcKgW0gByK3CkHoAta7GIpmKwcSgsVQCGUhKzMssyhdawEAHFJXg_c0uPKdKFuMWyNx9rsCz4sDYa-to0zlmlWZFJRzaXErNQljm9B6ZQc9a0eWfcHVjcUrSutW_cBm3_Q_511_WmWfmMyzrgSfATcHgHBfw0u9qato3VNg2vnh2i4pFJoLtRO6-4waoOPMbjqV4ZRs7fLHO0yVJnRrnHj5u91v_M_5ohvSOGPuQ</recordid><startdate>20200424</startdate><enddate>20200424</enddate><creator>Zischka, Hans</creator><creator>Kroemer, Guido</creator><general>Shared Science Publishers OG</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20200424</creationdate><title>Copper - a novel stimulator of autophagy</title><author>Zischka, Hans ; Kroemer, Guido</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-accbf6f26f560b696b9e5e668b0b5e66d314fea4c6f66b35467d777eace1d6663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>and Thoughts</topic><topic>Autophagy</topic><topic>Cancer</topic><topic>Copper</topic><topic>mek1</topic><topic>ulk1</topic><topic>ulk2</topic><topic>Wilson Disease</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zischka, Hans</creatorcontrib><creatorcontrib>Kroemer, Guido</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cell Stress</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zischka, Hans</au><au>Kroemer, Guido</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Copper - a novel stimulator of autophagy</atitle><jtitle>Cell Stress</jtitle><addtitle>Cell Stress</addtitle><date>2020-04-24</date><risdate>2020</risdate><volume>4</volume><issue>5</issue><spage>92</spage><epage>94</epage><pages>92-94</pages><issn>2523-0204</issn><eissn>2523-0204</eissn><abstract>Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang (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.</abstract><cop>Austria</cop><pub>Shared Science Publishers OG</pub><pmid>32420529</pmid><doi>10.15698/cst2020.05.218</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 2523-0204
ispartof Cell Stress, 2020-04, Vol.4 (5), p.92-94
issn 2523-0204
2523-0204
language eng
recordid cdi_doaj_primary_oai_doaj_org_article_c181b74508244a7d8da569a4e5426fc8
source Open Access: PubMed Central
subjects and Thoughts
Autophagy
Cancer
Copper
mek1
ulk1
ulk2
Wilson Disease
title Copper - a novel stimulator of autophagy
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T06%3A51%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Copper%20-%20a%20novel%20stimulator%20of%20autophagy&rft.jtitle=Cell%20Stress&rft.au=Zischka,%20Hans&rft.date=2020-04-24&rft.volume=4&rft.issue=5&rft.spage=92&rft.epage=94&rft.pages=92-94&rft.issn=2523-0204&rft.eissn=2523-0204&rft_id=info:doi/10.15698/cst2020.05.218&rft_dat=%3Cproquest_doaj_%3E2404382358%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c459t-accbf6f26f560b696b9e5e668b0b5e66d314fea4c6f66b35467d777eace1d6663%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2404382358&rft_id=info:pmid/32420529&rfr_iscdi=true