Parkin mediates neuroprotection through activation of Notch1 signaling

Parkin mediates neuroprotection through activation of Notch1 signaling

Parkin, an E3 ubiquitin ligase, is the most frequently mutated gene in hereditary Parkinson's disease. Inactivation of Parkin leads to impairment of the ubiquitin-proteasome system, resulting in the accumulation of misfolded or aggregated proteins and ensuing neurodegeneration. In this study, w...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neuroreport 2017-03, Vol.28 (4), p.181-186
Hauptverfasser: Yoon, Ji-Hye, Ann, Eun-Jung, Kim, Mi-Yeon, Ahn, Ji-Seon, Jo, Eun-Hye, Lee, Hye-Jin, Lee, Hye-Won, Lee, Young Chul, Kim, Jeong-Sun, Park, Hee-Sae
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 186
container_issue 4
container_start_page 181
container_title Neuroreport
container_volume 28
creator Yoon, Ji-Hye
Ann, Eun-Jung
Kim, Mi-Yeon
Ahn, Ji-Seon
Jo, Eun-Hye
Lee, Hye-Jin
Lee, Hye-Won
Lee, Young Chul
Kim, Jeong-Sun
Park, Hee-Sae
description Parkin, an E3 ubiquitin ligase, is the most frequently mutated gene in hereditary Parkinson's disease. Inactivation of Parkin leads to impairment of the ubiquitin-proteasome system, resulting in the accumulation of misfolded or aggregated proteins and ensuing neurodegeneration. In this study, we show that Parkin positively regulates the Notch1 signaling pathway. Overexpression of Parkin stabilized Notch1-IC protein levels, whereas knockdown of Parkin decreased Notch1-IC protein stability. Notably, overexpression of Parkin disrupted oxidative stress-induced apoptosis in neuronal cells. However, knockdown of Notch1 inhibited Parkin-induced neuronal cell survival. Together, these results indicate that Parkin is a novel regulator of the Notch1 signaling pathway, which promotes neuronal cell survival.
doi_str_mv 10.1097/WNR.0000000000000726
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1865816980</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1865816980</sourcerecordid><originalsourceid>FETCH-LOGICAL-c307t-ce3e428a1fab464557378676ac7f5e22b1b20f6a8065947b38627087ec615df43</originalsourceid><addsrcrecordid>eNpdkE1LAzEQhoMotlb_gcgevWxNsvk8SrEqlCqi6C1k0-x2dbupSVbw35vaKuJchhnedz4eAE4RHCMo-cXz_GEM_wbHbA8MEeFFTql42QdDKKnMiWR0AI5CeE0aCZE4BAMsEJOS4SGY3mv_1nTZyi4aHW3IOtt7t_YuWhMb12Vx6V1fLzOdyg_93XJVNnfRLFEWmrrTbdPVx-Cg0m2wJ7s8Ak_Tq8fJTT67u76dXM5yU0Aec2MLS7DQqNIlYYRSXnDBONOGV9RiXKISw4ppARmVhJeFYJhDwa1hiC4qUozA-XZuuvC9tyGqVROMbVvdWdcHhQSjm98ETFKylRrvQvC2UmvfrLT_VAiqDUGVCKr_BJPtbLehLxOUX9MPsuILBGZrsA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1865816980</pqid></control><display><type>article</type><title>Parkin mediates neuroprotection through activation of Notch1 signaling</title><source>Journals@Ovid Complete</source><creator>Yoon, Ji-Hye ; Ann, Eun-Jung ; Kim, Mi-Yeon ; Ahn, Ji-Seon ; Jo, Eun-Hye ; Lee, Hye-Jin ; Lee, Hye-Won ; Lee, Young Chul ; Kim, Jeong-Sun ; Park, Hee-Sae</creator><creatorcontrib>Yoon, Ji-Hye ; Ann, Eun-Jung ; Kim, Mi-Yeon ; Ahn, Ji-Seon ; Jo, Eun-Hye ; Lee, Hye-Jin ; Lee, Hye-Won ; Lee, Young Chul ; Kim, Jeong-Sun ; Park, Hee-Sae</creatorcontrib><description>Parkin, an E3 ubiquitin ligase, is the most frequently mutated gene in hereditary Parkinson's disease. Inactivation of Parkin leads to impairment of the ubiquitin-proteasome system, resulting in the accumulation of misfolded or aggregated proteins and ensuing neurodegeneration. In this study, we show that Parkin positively regulates the Notch1 signaling pathway. Overexpression of Parkin stabilized Notch1-IC protein levels, whereas knockdown of Parkin decreased Notch1-IC protein stability. Notably, overexpression of Parkin disrupted oxidative stress-induced apoptosis in neuronal cells. However, knockdown of Notch1 inhibited Parkin-induced neuronal cell survival. Together, these results indicate that Parkin is a novel regulator of the Notch1 signaling pathway, which promotes neuronal cell survival.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/WNR.0000000000000726</identifier><identifier>PMID: 28169962</identifier><language>eng</language><publisher>England</publisher><ispartof>Neuroreport, 2017-03, Vol.28 (4), p.181-186</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c307t-ce3e428a1fab464557378676ac7f5e22b1b20f6a8065947b38627087ec615df43</citedby><cites>FETCH-LOGICAL-c307t-ce3e428a1fab464557378676ac7f5e22b1b20f6a8065947b38627087ec615df43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28169962$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoon, Ji-Hye</creatorcontrib><creatorcontrib>Ann, Eun-Jung</creatorcontrib><creatorcontrib>Kim, Mi-Yeon</creatorcontrib><creatorcontrib>Ahn, Ji-Seon</creatorcontrib><creatorcontrib>Jo, Eun-Hye</creatorcontrib><creatorcontrib>Lee, Hye-Jin</creatorcontrib><creatorcontrib>Lee, Hye-Won</creatorcontrib><creatorcontrib>Lee, Young Chul</creatorcontrib><creatorcontrib>Kim, Jeong-Sun</creatorcontrib><creatorcontrib>Park, Hee-Sae</creatorcontrib><title>Parkin mediates neuroprotection through activation of Notch1 signaling</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Parkin, an E3 ubiquitin ligase, is the most frequently mutated gene in hereditary Parkinson's disease. Inactivation of Parkin leads to impairment of the ubiquitin-proteasome system, resulting in the accumulation of misfolded or aggregated proteins and ensuing neurodegeneration. In this study, we show that Parkin positively regulates the Notch1 signaling pathway. Overexpression of Parkin stabilized Notch1-IC protein levels, whereas knockdown of Parkin decreased Notch1-IC protein stability. Notably, overexpression of Parkin disrupted oxidative stress-induced apoptosis in neuronal cells. However, knockdown of Notch1 inhibited Parkin-induced neuronal cell survival. Together, these results indicate that Parkin is a novel regulator of the Notch1 signaling pathway, which promotes neuronal cell survival.</description><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNpdkE1LAzEQhoMotlb_gcgevWxNsvk8SrEqlCqi6C1k0-x2dbupSVbw35vaKuJchhnedz4eAE4RHCMo-cXz_GEM_wbHbA8MEeFFTql42QdDKKnMiWR0AI5CeE0aCZE4BAMsEJOS4SGY3mv_1nTZyi4aHW3IOtt7t_YuWhMb12Vx6V1fLzOdyg_93XJVNnfRLFEWmrrTbdPVx-Cg0m2wJ7s8Ak_Tq8fJTT67u76dXM5yU0Aec2MLS7DQqNIlYYRSXnDBONOGV9RiXKISw4ppARmVhJeFYJhDwa1hiC4qUozA-XZuuvC9tyGqVROMbVvdWdcHhQSjm98ETFKylRrvQvC2UmvfrLT_VAiqDUGVCKr_BJPtbLehLxOUX9MPsuILBGZrsA</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Yoon, Ji-Hye</creator><creator>Ann, Eun-Jung</creator><creator>Kim, Mi-Yeon</creator><creator>Ahn, Ji-Seon</creator><creator>Jo, Eun-Hye</creator><creator>Lee, Hye-Jin</creator><creator>Lee, Hye-Won</creator><creator>Lee, Young Chul</creator><creator>Kim, Jeong-Sun</creator><creator>Park, Hee-Sae</creator><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170301</creationdate><title>Parkin mediates neuroprotection through activation of Notch1 signaling</title><author>Yoon, Ji-Hye ; Ann, Eun-Jung ; Kim, Mi-Yeon ; Ahn, Ji-Seon ; Jo, Eun-Hye ; Lee, Hye-Jin ; Lee, Hye-Won ; Lee, Young Chul ; Kim, Jeong-Sun ; Park, Hee-Sae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c307t-ce3e428a1fab464557378676ac7f5e22b1b20f6a8065947b38627087ec615df43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Ji-Hye</creatorcontrib><creatorcontrib>Ann, Eun-Jung</creatorcontrib><creatorcontrib>Kim, Mi-Yeon</creatorcontrib><creatorcontrib>Ahn, Ji-Seon</creatorcontrib><creatorcontrib>Jo, Eun-Hye</creatorcontrib><creatorcontrib>Lee, Hye-Jin</creatorcontrib><creatorcontrib>Lee, Hye-Won</creatorcontrib><creatorcontrib>Lee, Young Chul</creatorcontrib><creatorcontrib>Kim, Jeong-Sun</creatorcontrib><creatorcontrib>Park, Hee-Sae</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoon, Ji-Hye</au><au>Ann, Eun-Jung</au><au>Kim, Mi-Yeon</au><au>Ahn, Ji-Seon</au><au>Jo, Eun-Hye</au><au>Lee, Hye-Jin</au><au>Lee, Hye-Won</au><au>Lee, Young Chul</au><au>Kim, Jeong-Sun</au><au>Park, Hee-Sae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Parkin mediates neuroprotection through activation of Notch1 signaling</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>28</volume><issue>4</issue><spage>181</spage><epage>186</epage><pages>181-186</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Parkin, an E3 ubiquitin ligase, is the most frequently mutated gene in hereditary Parkinson's disease. Inactivation of Parkin leads to impairment of the ubiquitin-proteasome system, resulting in the accumulation of misfolded or aggregated proteins and ensuing neurodegeneration. In this study, we show that Parkin positively regulates the Notch1 signaling pathway. Overexpression of Parkin stabilized Notch1-IC protein levels, whereas knockdown of Parkin decreased Notch1-IC protein stability. Notably, overexpression of Parkin disrupted oxidative stress-induced apoptosis in neuronal cells. However, knockdown of Notch1 inhibited Parkin-induced neuronal cell survival. Together, these results indicate that Parkin is a novel regulator of the Notch1 signaling pathway, which promotes neuronal cell survival.</abstract><cop>England</cop><pmid>28169962</pmid><doi>10.1097/WNR.0000000000000726</doi><tpages>6</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0959-4965
ispartof Neuroreport, 2017-03, Vol.28 (4), p.181-186
issn 0959-4965
1473-558X
language eng
recordid cdi_proquest_miscellaneous_1865816980
source Journals@Ovid Complete
title Parkin mediates neuroprotection through activation of Notch1 signaling
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T16%3A27%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Parkin%20mediates%20neuroprotection%20through%20activation%20of%20Notch1%20signaling&rft.jtitle=Neuroreport&rft.au=Yoon,%20Ji-Hye&rft.date=2017-03-01&rft.volume=28&rft.issue=4&rft.spage=181&rft.epage=186&rft.pages=181-186&rft.issn=0959-4965&rft.eissn=1473-558X&rft_id=info:doi/10.1097/WNR.0000000000000726&rft_dat=%3Cproquest_cross%3E1865816980%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1865816980&rft_id=info:pmid/28169962&rfr_iscdi=true