The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm
It is generally accepted that nitric oxide (NO) or its derivatives, reactive nitrogen species (RNS), are involved in the development of Parkinson's disease (PD). Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons....
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description | It is generally accepted that nitric oxide (NO) or its derivatives, reactive nitrogen species (RNS), are involved in the development of Parkinson's disease (PD). Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons. In this study, SH-SY5Y cells treated with rotenone were used as a model of neuronal death in PD. The treated cells underwent significant apoptosis, which was accompanied by an increase in intracellular NO in a rotenone dose-dependent manner. The CyDye switch approach was employed to screen for changes in S-nitrosylated (SNO) proteins in response to the rotenone treatment. Seven proteins with increased S-nitrosylation were identified in the treated SH-SY5Y cells, which included proliferating cell nuclear antigen (PCNA). Although PCNA is generally located in the nucleus and participates in DNA replication and repair, significant PCNA was identified in the SH-SY5Y cytosol. Using immunoprecipitation and pull-down approaches, PCNA was found to interact with caspase-9; using mass spectrometry, the two cysteine residues PCNA-Cys81 and -Cys162 were identified as candidate S-nitrosylated residues. In addition, the evidence obtained from in vitro and the cell model studies indicated that the S-nitrosylation of PCNA-Cys81 affected the interaction between PCNA and caspase-9. Furthermore, the interaction of PCNA and caspase-9 partially blocked caspase-9 activation, indicating that the S-nitrosylation of cytosolic PCNA may be a mediator of the apoptotic pathway. |
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Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons. In this study, SH-SY5Y cells treated with rotenone were used as a model of neuronal death in PD. The treated cells underwent significant apoptosis, which was accompanied by an increase in intracellular NO in a rotenone dose-dependent manner. The CyDye switch approach was employed to screen for changes in S-nitrosylated (SNO) proteins in response to the rotenone treatment. Seven proteins with increased S-nitrosylation were identified in the treated SH-SY5Y cells, which included proliferating cell nuclear antigen (PCNA). Although PCNA is generally located in the nucleus and participates in DNA replication and repair, significant PCNA was identified in the SH-SY5Y cytosol. Using immunoprecipitation and pull-down approaches, PCNA was found to interact with caspase-9; using mass spectrometry, the two cysteine residues PCNA-Cys81 and -Cys162 were identified as candidate S-nitrosylated residues. In addition, the evidence obtained from in vitro and the cell model studies indicated that the S-nitrosylation of PCNA-Cys81 affected the interaction between PCNA and caspase-9. Furthermore, the interaction of PCNA and caspase-9 partially blocked caspase-9 activation, indicating that the S-nitrosylation of cytosolic PCNA may be a mediator of the apoptotic pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0117546</identifier><identifier>PMID: 25675097</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Apoptosis ; Caspase ; Caspase 9 - metabolism ; Caspase-9 ; Cell Line, Tumor ; Cysteine ; Cytosol ; Cytosol - metabolism ; Deoxyribonucleic acid ; DNA ; DNA biosynthesis ; DNA repair ; DNA replication ; Enzyme Activation ; Humans ; Immunoprecipitation ; Kinases ; Mass spectrometry ; Mass spectroscopy ; Models, Molecular ; Movement disorders ; Neurodegeneration ; Neurodegenerative diseases ; Neurophysiology ; Nitric oxide ; Nitric Oxide - metabolism ; Nuclei (cytology) ; Oxidative Stress - drug effects ; Parkinson Disease - metabolism ; Parkinson's disease ; Proliferating cell nuclear antigen ; Proliferating Cell Nuclear Antigen - chemistry ; Proliferating Cell Nuclear Antigen - metabolism ; Protein Binding ; Protein Conformation ; Protein S ; Protein Transport ; Proteins ; Proteome ; Proteomics - methods ; Reactive nitrogen species ; Residues ; Rodents ; Rotenone ; Rotenone - pharmacology ; Signal Transduction</subject><ispartof>PloS one, 2015-02, Vol.10 (2), p.e0117546</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Yin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Yin et al 2015 Yin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-164c0e28c994c26c5a7a4123db049418d05794ebcbf699247c256bbaffee96773</citedby><cites>FETCH-LOGICAL-c692t-164c0e28c994c26c5a7a4123db049418d05794ebcbf699247c256bbaffee96773</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326459/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326459/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2101,2927,23865,27923,27924,53790,53792,79471,79472</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25675097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ariga, Hiroyoshi</contributor><creatorcontrib>Yin, Liang</creatorcontrib><creatorcontrib>Xie, Yingying</creatorcontrib><creatorcontrib>Yin, Songyue</creatorcontrib><creatorcontrib>Lv, Xiaolei</creatorcontrib><creatorcontrib>Zhang, Jia</creatorcontrib><creatorcontrib>Gu, Zezong</creatorcontrib><creatorcontrib>Sun, Haidan</creatorcontrib><creatorcontrib>Liu, Siqi</creatorcontrib><title>The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>It is generally accepted that nitric oxide (NO) or its derivatives, reactive nitrogen species (RNS), are involved in the development of Parkinson's disease (PD). Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons. In this study, SH-SY5Y cells treated with rotenone were used as a model of neuronal death in PD. The treated cells underwent significant apoptosis, which was accompanied by an increase in intracellular NO in a rotenone dose-dependent manner. The CyDye switch approach was employed to screen for changes in S-nitrosylated (SNO) proteins in response to the rotenone treatment. Seven proteins with increased S-nitrosylation were identified in the treated SH-SY5Y cells, which included proliferating cell nuclear antigen (PCNA). Although PCNA is generally located in the nucleus and participates in DNA replication and repair, significant PCNA was identified in the SH-SY5Y cytosol. Using immunoprecipitation and pull-down approaches, PCNA was found to interact with caspase-9; using mass spectrometry, the two cysteine residues PCNA-Cys81 and -Cys162 were identified as candidate S-nitrosylated residues. In addition, the evidence obtained from in vitro and the cell model studies indicated that the S-nitrosylation of PCNA-Cys81 affected the interaction between PCNA and caspase-9. Furthermore, the interaction of PCNA and caspase-9 partially blocked caspase-9 activation, indicating that the S-nitrosylation of cytosolic PCNA may be a mediator of the apoptotic pathway.</description><subject>Analysis</subject><subject>Apoptosis</subject><subject>Caspase</subject><subject>Caspase 9 - metabolism</subject><subject>Caspase-9</subject><subject>Cell Line, Tumor</subject><subject>Cysteine</subject><subject>Cytosol</subject><subject>Cytosol - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA biosynthesis</subject><subject>DNA repair</subject><subject>DNA replication</subject><subject>Enzyme Activation</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Kinases</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Models, Molecular</subject><subject>Movement disorders</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurophysiology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nuclei (cytology)</subject><subject>Oxidative Stress - drug effects</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson's disease</subject><subject>Proliferating cell nuclear antigen</subject><subject>Proliferating Cell Nuclear Antigen - chemistry</subject><subject>Proliferating Cell Nuclear Antigen - metabolism</subject><subject>Protein Binding</subject><subject>Protein Conformation</subject><subject>Protein S</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Proteome</subject><subject>Proteomics - methods</subject><subject>Reactive nitrogen species</subject><subject>Residues</subject><subject>Rodents</subject><subject>Rotenone</subject><subject>Rotenone - pharmacology</subject><subject>Signal Transduction</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBYmsTHRYvtOE59g1RVfFSa2MQGt9aJ47QuThxih1F-Pe6aTQ3aBcqFI_t5X59zfE6SPCd4StKcvNu4vmvATlvX6CkmJM8Yf5AcE5HSCac4fXjwf5Q88X6DcZbOOH-cHNGM5xkW-XFyfbXW6HLSmNA5v7UQjGuQDxB6j1yFLhZf5sg6Bdb80SUyDVLb4LyzyNQtqOBRiHpoXRtcMAq1ENbXsN2BgC6g-2Ea75rXHpXGa_A6Ah2UZlU_TR5VYL1-NqwnybePH64Wnydn55-Wi_nZRHFBw4RwprCmMyUEU5SrDHJghKZlgZlgZFbiLBdMF6qouBCU5SqmVhRQVVoLnufpSfJy79ta5-VQMy8Jz5hIGeMiEss9UTrYyLYzNXRb6cDImw3XrSR0MTerZc5IRTEtMNYpK9NqlokYpsaU0kIrnkav98NtfVHrUukmdGBHpuOTxqzlyv2SLKWcZbtg3gwGnfvZax9kbbzS1kKjXX8TN8csoiyip_-g92c3UCuICZimcvFetTOVc0azWawZo5Ga3kPFr9S1UbHBKhP3R4K3I0Fkgv4dVtB7L5eXX_-fPf8-Zl8dsGsNNqxjt_W7tvRjkO1BFfvWd7q6KzLBcjcft9WQu_mQw3xE2YvDB7oT3Q5E-hfBrgrm</recordid><startdate>20150212</startdate><enddate>20150212</enddate><creator>Yin, Liang</creator><creator>Xie, Yingying</creator><creator>Yin, Songyue</creator><creator>Lv, Xiaolei</creator><creator>Zhang, Jia</creator><creator>Gu, Zezong</creator><creator>Sun, Haidan</creator><creator>Liu, Siqi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150212</creationdate><title>The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm</title><author>Yin, Liang ; Xie, Yingying ; Yin, Songyue ; Lv, Xiaolei ; Zhang, Jia ; Gu, Zezong ; Sun, Haidan ; Liu, Siqi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-164c0e28c994c26c5a7a4123db049418d05794ebcbf699247c256bbaffee96773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Apoptosis</topic><topic>Caspase</topic><topic>Caspase 9 - metabolism</topic><topic>Caspase-9</topic><topic>Cell Line, Tumor</topic><topic>Cysteine</topic><topic>Cytosol</topic><topic>Cytosol - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA biosynthesis</topic><topic>DNA repair</topic><topic>DNA replication</topic><topic>Enzyme Activation</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Kinases</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Models, Molecular</topic><topic>Movement disorders</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neurophysiology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nuclei (cytology)</topic><topic>Oxidative Stress - drug effects</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson's disease</topic><topic>Proliferating cell nuclear antigen</topic><topic>Proliferating Cell Nuclear Antigen - chemistry</topic><topic>Proliferating Cell Nuclear Antigen - metabolism</topic><topic>Protein Binding</topic><topic>Protein Conformation</topic><topic>Protein S</topic><topic>Protein Transport</topic><topic>Proteins</topic><topic>Proteome</topic><topic>Proteomics - methods</topic><topic>Reactive nitrogen species</topic><topic>Residues</topic><topic>Rodents</topic><topic>Rotenone</topic><topic>Rotenone - pharmacology</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Liang</creatorcontrib><creatorcontrib>Xie, Yingying</creatorcontrib><creatorcontrib>Yin, Songyue</creatorcontrib><creatorcontrib>Lv, Xiaolei</creatorcontrib><creatorcontrib>Zhang, Jia</creatorcontrib><creatorcontrib>Gu, Zezong</creatorcontrib><creatorcontrib>Sun, Haidan</creatorcontrib><creatorcontrib>Liu, Siqi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Liang</au><au>Xie, Yingying</au><au>Yin, Songyue</au><au>Lv, Xiaolei</au><au>Zhang, Jia</au><au>Gu, Zezong</au><au>Sun, Haidan</au><au>Liu, Siqi</au><au>Ariga, Hiroyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-02-12</date><risdate>2015</risdate><volume>10</volume><issue>2</issue><spage>e0117546</spage><pages>e0117546-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>It is generally accepted that nitric oxide (NO) or its derivatives, reactive nitrogen species (RNS), are involved in the development of Parkinson's disease (PD). Recently, emerging evidence in the study of PD has indicated that protein S-nitrosylation triggers the signaling changes in neurons. In this study, SH-SY5Y cells treated with rotenone were used as a model of neuronal death in PD. The treated cells underwent significant apoptosis, which was accompanied by an increase in intracellular NO in a rotenone dose-dependent manner. The CyDye switch approach was employed to screen for changes in S-nitrosylated (SNO) proteins in response to the rotenone treatment. Seven proteins with increased S-nitrosylation were identified in the treated SH-SY5Y cells, which included proliferating cell nuclear antigen (PCNA). Although PCNA is generally located in the nucleus and participates in DNA replication and repair, significant PCNA was identified in the SH-SY5Y cytosol. Using immunoprecipitation and pull-down approaches, PCNA was found to interact with caspase-9; using mass spectrometry, the two cysteine residues PCNA-Cys81 and -Cys162 were identified as candidate S-nitrosylated residues. In addition, the evidence obtained from in vitro and the cell model studies indicated that the S-nitrosylation of PCNA-Cys81 affected the interaction between PCNA and caspase-9. Furthermore, the interaction of PCNA and caspase-9 partially blocked caspase-9 activation, indicating that the S-nitrosylation of cytosolic PCNA may be a mediator of the apoptotic pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25675097</pmid><doi>10.1371/journal.pone.0117546</doi><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Apoptosis Caspase Caspase 9 - metabolism Caspase-9 Cell Line, Tumor Cysteine Cytosol Cytosol - metabolism Deoxyribonucleic acid DNA DNA biosynthesis DNA repair DNA replication Enzyme Activation Humans Immunoprecipitation Kinases Mass spectrometry Mass spectroscopy Models, Molecular Movement disorders Neurodegeneration Neurodegenerative diseases Neurophysiology Nitric oxide Nitric Oxide - metabolism Nuclei (cytology) Oxidative Stress - drug effects Parkinson Disease - metabolism Parkinson's disease Proliferating cell nuclear antigen Proliferating Cell Nuclear Antigen - chemistry Proliferating Cell Nuclear Antigen - metabolism Protein Binding Protein Conformation Protein S Protein Transport Proteins Proteome Proteomics - methods Reactive nitrogen species Residues Rodents Rotenone Rotenone - pharmacology Signal Transduction |
title | The S-nitrosylation status of PCNA localized in cytosol impacts the apoptotic pathway in a Parkinson's disease paradigm |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T19%3A01%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20S-nitrosylation%20status%20of%20PCNA%20localized%20in%20cytosol%20impacts%20the%20apoptotic%20pathway%20in%20a%20Parkinson's%20disease%20paradigm&rft.jtitle=PloS%20one&rft.au=Yin,%20Liang&rft.date=2015-02-12&rft.volume=10&rft.issue=2&rft.spage=e0117546&rft.pages=e0117546-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0117546&rft_dat=%3Cgale_plos_%3EA425892442%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1654934469&rft_id=info:pmid/25675097&rft_galeid=A425892442&rft_doaj_id=oai_doaj_org_article_741f202b00e34d3f859c69e0222bec63&rfr_iscdi=true |