Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons
Inhibitor of apoptosis stimulating protein of p53 (iASPP) is related to the pathogenesis of several neurological disorders by affecting the oxidative stress and survival of neurons. However, whether iASPP has a role in Parkinson disease (PD) remains to be determined. This work explored the potential...
Gespeichert in:
| Veröffentlicht in: | Metabolic brain disease 2024-06, Vol.39 (5), p.871-884 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 884 |
|---|---|
| container_issue | 5 |
| container_start_page | 871 |
| container_title | Metabolic brain disease |
| container_volume | 39 |
| creator | Chen, Lei Duan, Fengju Ge, Fangfang Tian, Lu Li, Yuanyuan Li, Ying Zhu, Qing Zhou, Qiong Lin, Hong |
| description | Inhibitor of apoptosis stimulating protein of p53 (iASPP) is related to the pathogenesis of several neurological disorders by affecting the oxidative stress and survival of neurons. However, whether iASPP has a role in Parkinson disease (PD) remains to be determined. This work explored the potential regulatory effect of iASPP in an in vitro model of PD based on 1-methyl-4-phenylpyridinium (MPP
+
)-evoked neurotoxicity of dopaminergic neurons in culture. MN9D neurons were treated with MPP
+
at 200 µM in the culture media for 24 h to induce neurotoxicity. Overexpression and silencing of iASPP in neurons were achieved by infecting recombinant adenovirus expressing iASPP and sh-iASPP, respectively. Protein expression was examined by immunoblotting. MPP
+
-evoked neurotoxicity of dopaminergic neurons was determined by cell viability, TUNEL, and flow cytometric assays. The transcriptional activity of nuclear erythroid factor 2-like 2 (Nrf2) was assessed by luciferase reporter assay. Kelch-like ECH-associated protein 1 (Keap1)-knockout neurons were generated by lentiCRISPR/Cas9-Keap1 constructs. Expression levels of iASPP declined in MPP
+
-stimulated neurons. Overexpression of iASPP in neurons exhibited inhibitory effects on MPP
+
-evoked apoptosis, α-synuclein accumulation, and oxidative stress, while iASPP-deficient neurons were more sensitive to MPP
+
-induced neurotoxicity. Overexpression of iASPP led to an enhancing effect on Nrf2 activation in MPP
+
-stimulated neurons. Mechanism research revealed that iASPP may contribute to the activation of Nrf2 by competing with Nrf2 in binding with Keap1. Notably, the regulatory effect of iASPP on Nrf2 was diminished in Keap1-knockout neurons. The chemical inhibition of Nrf2 or knockdown of Nrf2 abrogated the protective effects of iASPP on MPP
+
-induced neurotoxicity. To conclude, iASPP protects dopaminergic neurons against MPP
+
-induced neurotoxicity through modulation of the Keap1/Nrf2 axis. Therefore, iASPP may play a crucial role in mediating the loss of dopaminergic neurons in PD, and targeting the iASPP-Nrf2 axis could be a promising strategy for treating PD. |
| doi_str_mv | 10.1007/s11011-024-01367-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3065271726</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3065271726</sourcerecordid><originalsourceid>FETCH-LOGICAL-c256t-445f3ee0033c3b435a034df9afe807063a51f073c4b38b9927fccb9e23814b9a3</originalsourceid><addsrcrecordid>eNp9kU1P3DAYhC1UBNuFP9BDFakXpCpg-43t5Fih0q60CA5wthzH2Rpt7NR2pO6_x0v4qDhwsq15ZjzSIPSF4HOCsbiIhGBCSkyrEhPgotwdoAVhAkoBnH36736MPsf4gDEGRpojdAx1XVHO6QJNK_fHtjb5UPi-UKMfk482FjHZYdqqZN2mGINPxro9MDKYnzrFQm2UdTEV17e330vrukmbrnBmyrr_Z7VNu72l86MarDNhY_WsuniCDnu1jeb0-Vyi-6ufd5e_y_XNr9Xlj3WpKeOprCrWgzG5NmhoK2AKQ9X1jepNjQXmoBjpsQBdtVC3TUNFr3XbGAo1qdpGwRKdzbm589_JxCQHG7XZbpUzfooSMGdUEEF5Rr-9Qx_8FFxulykhmCAcSKboTOngYwyml2Owgwo7SbDcjyLnUWQeRT6NInfZ9PU5emoH071aXlbIAMxAzJLbmPD29wexjzxgmSA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3077571631</pqid></control><display><type>article</type><title>Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons</title><source>SpringerLink Journals - AutoHoldings</source><creator>Chen, Lei ; Duan, Fengju ; Ge, Fangfang ; Tian, Lu ; Li, Yuanyuan ; Li, Ying ; Zhu, Qing ; Zhou, Qiong ; Lin, Hong</creator><creatorcontrib>Chen, Lei ; Duan, Fengju ; Ge, Fangfang ; Tian, Lu ; Li, Yuanyuan ; Li, Ying ; Zhu, Qing ; Zhou, Qiong ; Lin, Hong</creatorcontrib><description>Inhibitor of apoptosis stimulating protein of p53 (iASPP) is related to the pathogenesis of several neurological disorders by affecting the oxidative stress and survival of neurons. However, whether iASPP has a role in Parkinson disease (PD) remains to be determined. This work explored the potential regulatory effect of iASPP in an in vitro model of PD based on 1-methyl-4-phenylpyridinium (MPP
+
)-evoked neurotoxicity of dopaminergic neurons in culture. MN9D neurons were treated with MPP
+
at 200 µM in the culture media for 24 h to induce neurotoxicity. Overexpression and silencing of iASPP in neurons were achieved by infecting recombinant adenovirus expressing iASPP and sh-iASPP, respectively. Protein expression was examined by immunoblotting. MPP
+
-evoked neurotoxicity of dopaminergic neurons was determined by cell viability, TUNEL, and flow cytometric assays. The transcriptional activity of nuclear erythroid factor 2-like 2 (Nrf2) was assessed by luciferase reporter assay. Kelch-like ECH-associated protein 1 (Keap1)-knockout neurons were generated by lentiCRISPR/Cas9-Keap1 constructs. Expression levels of iASPP declined in MPP
+
-stimulated neurons. Overexpression of iASPP in neurons exhibited inhibitory effects on MPP
+
-evoked apoptosis, α-synuclein accumulation, and oxidative stress, while iASPP-deficient neurons were more sensitive to MPP
+
-induced neurotoxicity. Overexpression of iASPP led to an enhancing effect on Nrf2 activation in MPP
+
-stimulated neurons. Mechanism research revealed that iASPP may contribute to the activation of Nrf2 by competing with Nrf2 in binding with Keap1. Notably, the regulatory effect of iASPP on Nrf2 was diminished in Keap1-knockout neurons. The chemical inhibition of Nrf2 or knockdown of Nrf2 abrogated the protective effects of iASPP on MPP
+
-induced neurotoxicity. To conclude, iASPP protects dopaminergic neurons against MPP
+
-induced neurotoxicity through modulation of the Keap1/Nrf2 axis. Therefore, iASPP may play a crucial role in mediating the loss of dopaminergic neurons in PD, and targeting the iASPP-Nrf2 axis could be a promising strategy for treating PD.</description><identifier>ISSN: 1573-7365</identifier><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-024-01367-y</identifier><identifier>PMID: 38842662</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell culture ; Cell viability ; Culture media ; Dopamine receptors ; Flow cytometry ; Immunoblotting ; Inhibitors ; Metabolic Diseases ; Movement disorders ; MPP ; Neurodegenerative diseases ; Neurogenesis ; Neurological diseases ; Neurology ; Neuromodulation ; Neurons ; Neurosciences ; Neurotoxicity ; Oncology ; Original Article ; Oxidative stress ; p53 Protein ; Parkinson's disease ; Pathogenesis ; Proteins ; Synuclein</subject><ispartof>Metabolic brain disease, 2024-06, Vol.39 (5), p.871-884</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-445f3ee0033c3b435a034df9afe807063a51f073c4b38b9927fccb9e23814b9a3</cites><orcidid>0009-0005-7469-8637 ; 0000-0001-6702-0127 ; 0009-0000-2118-5647 ; 0009-0002-5202-5958 ; 0009-0003-8440-3287 ; 0009-0002-1154-8867 ; 0009-0007-1156-0969 ; 0009-0004-8645-4528 ; 0009-0006-4508-123X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11011-024-01367-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-024-01367-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38842662$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Duan, Fengju</creatorcontrib><creatorcontrib>Ge, Fangfang</creatorcontrib><creatorcontrib>Tian, Lu</creatorcontrib><creatorcontrib>Li, Yuanyuan</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhu, Qing</creatorcontrib><creatorcontrib>Zhou, Qiong</creatorcontrib><creatorcontrib>Lin, Hong</creatorcontrib><title>Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><addtitle>Metab Brain Dis</addtitle><description>Inhibitor of apoptosis stimulating protein of p53 (iASPP) is related to the pathogenesis of several neurological disorders by affecting the oxidative stress and survival of neurons. However, whether iASPP has a role in Parkinson disease (PD) remains to be determined. This work explored the potential regulatory effect of iASPP in an in vitro model of PD based on 1-methyl-4-phenylpyridinium (MPP
+
)-evoked neurotoxicity of dopaminergic neurons in culture. MN9D neurons were treated with MPP
+
at 200 µM in the culture media for 24 h to induce neurotoxicity. Overexpression and silencing of iASPP in neurons were achieved by infecting recombinant adenovirus expressing iASPP and sh-iASPP, respectively. Protein expression was examined by immunoblotting. MPP
+
-evoked neurotoxicity of dopaminergic neurons was determined by cell viability, TUNEL, and flow cytometric assays. The transcriptional activity of nuclear erythroid factor 2-like 2 (Nrf2) was assessed by luciferase reporter assay. Kelch-like ECH-associated protein 1 (Keap1)-knockout neurons were generated by lentiCRISPR/Cas9-Keap1 constructs. Expression levels of iASPP declined in MPP
+
-stimulated neurons. Overexpression of iASPP in neurons exhibited inhibitory effects on MPP
+
-evoked apoptosis, α-synuclein accumulation, and oxidative stress, while iASPP-deficient neurons were more sensitive to MPP
+
-induced neurotoxicity. Overexpression of iASPP led to an enhancing effect on Nrf2 activation in MPP
+
-stimulated neurons. Mechanism research revealed that iASPP may contribute to the activation of Nrf2 by competing with Nrf2 in binding with Keap1. Notably, the regulatory effect of iASPP on Nrf2 was diminished in Keap1-knockout neurons. The chemical inhibition of Nrf2 or knockdown of Nrf2 abrogated the protective effects of iASPP on MPP
+
-induced neurotoxicity. To conclude, iASPP protects dopaminergic neurons against MPP
+
-induced neurotoxicity through modulation of the Keap1/Nrf2 axis. Therefore, iASPP may play a crucial role in mediating the loss of dopaminergic neurons in PD, and targeting the iASPP-Nrf2 axis could be a promising strategy for treating PD.</description><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell culture</subject><subject>Cell viability</subject><subject>Culture media</subject><subject>Dopamine receptors</subject><subject>Flow cytometry</subject><subject>Immunoblotting</subject><subject>Inhibitors</subject><subject>Metabolic Diseases</subject><subject>Movement disorders</subject><subject>MPP</subject><subject>Neurodegenerative diseases</subject><subject>Neurogenesis</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neuromodulation</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>p53 Protein</subject><subject>Parkinson's disease</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Synuclein</subject><issn>1573-7365</issn><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kU1P3DAYhC1UBNuFP9BDFakXpCpg-43t5Fih0q60CA5wthzH2Rpt7NR2pO6_x0v4qDhwsq15ZjzSIPSF4HOCsbiIhGBCSkyrEhPgotwdoAVhAkoBnH36736MPsf4gDEGRpojdAx1XVHO6QJNK_fHtjb5UPi-UKMfk482FjHZYdqqZN2mGINPxro9MDKYnzrFQm2UdTEV17e330vrukmbrnBmyrr_Z7VNu72l86MarDNhY_WsuniCDnu1jeb0-Vyi-6ufd5e_y_XNr9Xlj3WpKeOprCrWgzG5NmhoK2AKQ9X1jepNjQXmoBjpsQBdtVC3TUNFr3XbGAo1qdpGwRKdzbm589_JxCQHG7XZbpUzfooSMGdUEEF5Rr-9Qx_8FFxulykhmCAcSKboTOngYwyml2Owgwo7SbDcjyLnUWQeRT6NInfZ9PU5emoH071aXlbIAMxAzJLbmPD29wexjzxgmSA</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Chen, Lei</creator><creator>Duan, Fengju</creator><creator>Ge, Fangfang</creator><creator>Tian, Lu</creator><creator>Li, Yuanyuan</creator><creator>Li, Ying</creator><creator>Zhu, Qing</creator><creator>Zhou, Qiong</creator><creator>Lin, Hong</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0005-7469-8637</orcidid><orcidid>https://orcid.org/0000-0001-6702-0127</orcidid><orcidid>https://orcid.org/0009-0000-2118-5647</orcidid><orcidid>https://orcid.org/0009-0002-5202-5958</orcidid><orcidid>https://orcid.org/0009-0003-8440-3287</orcidid><orcidid>https://orcid.org/0009-0002-1154-8867</orcidid><orcidid>https://orcid.org/0009-0007-1156-0969</orcidid><orcidid>https://orcid.org/0009-0004-8645-4528</orcidid><orcidid>https://orcid.org/0009-0006-4508-123X</orcidid></search><sort><creationdate>20240601</creationdate><title>Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons</title><author>Chen, Lei ; Duan, Fengju ; Ge, Fangfang ; Tian, Lu ; Li, Yuanyuan ; Li, Ying ; Zhu, Qing ; Zhou, Qiong ; Lin, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-445f3ee0033c3b435a034df9afe807063a51f073c4b38b9927fccb9e23814b9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell culture</topic><topic>Cell viability</topic><topic>Culture media</topic><topic>Dopamine receptors</topic><topic>Flow cytometry</topic><topic>Immunoblotting</topic><topic>Inhibitors</topic><topic>Metabolic Diseases</topic><topic>Movement disorders</topic><topic>MPP</topic><topic>Neurodegenerative diseases</topic><topic>Neurogenesis</topic><topic>Neurological diseases</topic><topic>Neurology</topic><topic>Neuromodulation</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>p53 Protein</topic><topic>Parkinson's disease</topic><topic>Pathogenesis</topic><topic>Proteins</topic><topic>Synuclein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Duan, Fengju</creatorcontrib><creatorcontrib>Ge, Fangfang</creatorcontrib><creatorcontrib>Tian, Lu</creatorcontrib><creatorcontrib>Li, Yuanyuan</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Zhu, Qing</creatorcontrib><creatorcontrib>Zhou, Qiong</creatorcontrib><creatorcontrib>Lin, Hong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Lei</au><au>Duan, Fengju</au><au>Ge, Fangfang</au><au>Tian, Lu</au><au>Li, Yuanyuan</au><au>Li, Ying</au><au>Zhu, Qing</au><au>Zhou, Qiong</au><au>Lin, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2024-06-01</date><risdate>2024</risdate><volume>39</volume><issue>5</issue><spage>871</spage><epage>884</epage><pages>871-884</pages><issn>1573-7365</issn><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>Inhibitor of apoptosis stimulating protein of p53 (iASPP) is related to the pathogenesis of several neurological disorders by affecting the oxidative stress and survival of neurons. However, whether iASPP has a role in Parkinson disease (PD) remains to be determined. This work explored the potential regulatory effect of iASPP in an in vitro model of PD based on 1-methyl-4-phenylpyridinium (MPP
+
)-evoked neurotoxicity of dopaminergic neurons in culture. MN9D neurons were treated with MPP
+
at 200 µM in the culture media for 24 h to induce neurotoxicity. Overexpression and silencing of iASPP in neurons were achieved by infecting recombinant adenovirus expressing iASPP and sh-iASPP, respectively. Protein expression was examined by immunoblotting. MPP
+
-evoked neurotoxicity of dopaminergic neurons was determined by cell viability, TUNEL, and flow cytometric assays. The transcriptional activity of nuclear erythroid factor 2-like 2 (Nrf2) was assessed by luciferase reporter assay. Kelch-like ECH-associated protein 1 (Keap1)-knockout neurons were generated by lentiCRISPR/Cas9-Keap1 constructs. Expression levels of iASPP declined in MPP
+
-stimulated neurons. Overexpression of iASPP in neurons exhibited inhibitory effects on MPP
+
-evoked apoptosis, α-synuclein accumulation, and oxidative stress, while iASPP-deficient neurons were more sensitive to MPP
+
-induced neurotoxicity. Overexpression of iASPP led to an enhancing effect on Nrf2 activation in MPP
+
-stimulated neurons. Mechanism research revealed that iASPP may contribute to the activation of Nrf2 by competing with Nrf2 in binding with Keap1. Notably, the regulatory effect of iASPP on Nrf2 was diminished in Keap1-knockout neurons. The chemical inhibition of Nrf2 or knockdown of Nrf2 abrogated the protective effects of iASPP on MPP
+
-induced neurotoxicity. To conclude, iASPP protects dopaminergic neurons against MPP
+
-induced neurotoxicity through modulation of the Keap1/Nrf2 axis. Therefore, iASPP may play a crucial role in mediating the loss of dopaminergic neurons in PD, and targeting the iASPP-Nrf2 axis could be a promising strategy for treating PD.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>38842662</pmid><doi>10.1007/s11011-024-01367-y</doi><tpages>14</tpages><orcidid>https://orcid.org/0009-0005-7469-8637</orcidid><orcidid>https://orcid.org/0000-0001-6702-0127</orcidid><orcidid>https://orcid.org/0009-0000-2118-5647</orcidid><orcidid>https://orcid.org/0009-0002-5202-5958</orcidid><orcidid>https://orcid.org/0009-0003-8440-3287</orcidid><orcidid>https://orcid.org/0009-0002-1154-8867</orcidid><orcidid>https://orcid.org/0009-0007-1156-0969</orcidid><orcidid>https://orcid.org/0009-0004-8645-4528</orcidid><orcidid>https://orcid.org/0009-0006-4508-123X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1573-7365 |
| ispartof | Metabolic brain disease, 2024-06, Vol.39 (5), p.871-884 |
| issn | 1573-7365 0885-7490 1573-7365 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3065271726 |
| source | SpringerLink Journals - AutoHoldings |
| subjects | Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Cell culture Cell viability Culture media Dopamine receptors Flow cytometry Immunoblotting Inhibitors Metabolic Diseases Movement disorders MPP Neurodegenerative diseases Neurogenesis Neurological diseases Neurology Neuromodulation Neurons Neurosciences Neurotoxicity Oncology Original Article Oxidative stress p53 Protein Parkinson's disease Pathogenesis Proteins Synuclein |
| title | Inhibitor of apoptosis stimulating protein of p53 protects against MPP+-induced neurotoxicity of dopaminergic neurons |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T14%3A01%3A41IST&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=Inhibitor%20of%20apoptosis%20stimulating%20protein%20of%20p53%20protects%20against%20MPP+-induced%20neurotoxicity%20of%20dopaminergic%20neurons&rft.jtitle=Metabolic%20brain%20disease&rft.au=Chen,%20Lei&rft.date=2024-06-01&rft.volume=39&rft.issue=5&rft.spage=871&rft.epage=884&rft.pages=871-884&rft.issn=1573-7365&rft.eissn=1573-7365&rft_id=info:doi/10.1007/s11011-024-01367-y&rft_dat=%3Cproquest_cross%3E3065271726%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=3077571631&rft_id=info:pmid/38842662&rfr_iscdi=true |