SOD1 stimulates lamellipodial protrusions in Neuro 2A cell lines
We here investigated the effects of overexpressed superoxide dismutase (SOD)1 and amyotrophic lateral sclerosis (ALS)-linked SOD1 mutants G93A and G147S in Neuro 2A (N2A) cell lines, and found a three-fold increase in lamellipodia either in cells cultured under differentiated or undifferentiated gro...
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| Veröffentlicht in: | Communicative & integrative biology 2018-05, Vol.11 (3), p.1-7 |
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| creator | Ferrari, Ilaria Verpelli, Chiara Crespi, Arianna Sala, Carlo Fornasari, Diego Pietrini, Grazia |
| description | We here investigated the effects of overexpressed superoxide dismutase (SOD)1 and amyotrophic lateral sclerosis (ALS)-linked SOD1 mutants G93A and G147S in Neuro 2A (N2A) cell lines, and found a three-fold increase in lamellipodia either in cells cultured under differentiated or undifferentiated growth conditions. In undifferentiated N2A cells, SOD1 constructs promoted lamellipodial protrusions to similar extent as the overexpression of Rac1, and SOD1-mediated lamellipodia were prevented by coexpression of the N17 dominant-negative form of Rac1, or shRNA for a downstream effector of Rac1, the insulin receptor tyrosine kinase substrate p53 (IRSp53) or its binding partner LIN7. Moreover, no additive effect was measured by coexpression of the SOD1 constructs with Rac1, IRSp53 or LIN7. Collectively these data support a role for SOD1 in the regulation of Rac1-mediated lamellipodia pathway, a property fully retained by the two SOD1 mutants. |
| doi_str_mv | 10.1080/19420889.2018.1486652 |
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In undifferentiated N2A cells, SOD1 constructs promoted lamellipodial protrusions to similar extent as the overexpression of Rac1, and SOD1-mediated lamellipodia were prevented by coexpression of the N17 dominant-negative form of Rac1, or shRNA for a downstream effector of Rac1, the insulin receptor tyrosine kinase substrate p53 (IRSp53) or its binding partner LIN7. Moreover, no additive effect was measured by coexpression of the SOD1 constructs with Rac1, IRSp53 or LIN7. Collectively these data support a role for SOD1 in the regulation of Rac1-mediated lamellipodia pathway, a property fully retained by the two SOD1 mutants.</description><identifier>ISSN: 1942-0889</identifier><identifier>EISSN: 1942-0889</identifier><identifier>DOI: 10.1080/19420889.2018.1486652</identifier><identifier>PMID: 30214670</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic lateral Sclerosis (ALS) ; Cell differentiation ; Cell lines ; Cellular biology ; Enzymes ; Growth conditions ; Insulin ; Insulin receptor substrate of 53 kDa (IRSp53) ; Lamellipodia ; LIN7 ; Mutants ; Mutation ; Neurobiology ; Protein-tyrosine kinase receptors ; Pseudopodia ; Rac1 GTPases ; Rac1 protein ; Research Paper ; SOD1 mutants G93A and G147S ; Substrates ; Superoxide dismutase ; Superoxide dismutase 1 (SOD1)</subject><ispartof>Communicative & integrative biology, 2018-05, Vol.11 (3), p.1-7</ispartof><rights>2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2018</rights><rights>2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2018 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4252-3acfd8265940bb805ac151536cf338630029b43ed2e2ea46a0ed6439b8e91b7c3</cites><orcidid>0000-0002-9668-3103 ; 0000-0002-2629-0347 ; 0000-0003-2949-9725 ; 0000-0003-0662-9523 ; 0000-0002-1148-8465</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132423/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132423/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,27502,27924,27925,53791,53793,59143,59144</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30214670$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferrari, Ilaria</creatorcontrib><creatorcontrib>Verpelli, Chiara</creatorcontrib><creatorcontrib>Crespi, Arianna</creatorcontrib><creatorcontrib>Sala, Carlo</creatorcontrib><creatorcontrib>Fornasari, Diego</creatorcontrib><creatorcontrib>Pietrini, Grazia</creatorcontrib><title>SOD1 stimulates lamellipodial protrusions in Neuro 2A cell lines</title><title>Communicative & integrative biology</title><addtitle>Commun Integr Biol</addtitle><description>We here investigated the effects of overexpressed superoxide dismutase (SOD)1 and amyotrophic lateral sclerosis (ALS)-linked SOD1 mutants G93A and G147S in Neuro 2A (N2A) cell lines, and found a three-fold increase in lamellipodia either in cells cultured under differentiated or undifferentiated growth conditions. In undifferentiated N2A cells, SOD1 constructs promoted lamellipodial protrusions to similar extent as the overexpression of Rac1, and SOD1-mediated lamellipodia were prevented by coexpression of the N17 dominant-negative form of Rac1, or shRNA for a downstream effector of Rac1, the insulin receptor tyrosine kinase substrate p53 (IRSp53) or its binding partner LIN7. Moreover, no additive effect was measured by coexpression of the SOD1 constructs with Rac1, IRSp53 or LIN7. Collectively these data support a role for SOD1 in the regulation of Rac1-mediated lamellipodia pathway, a property fully retained by the two SOD1 mutants.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic lateral Sclerosis (ALS)</subject><subject>Cell differentiation</subject><subject>Cell lines</subject><subject>Cellular biology</subject><subject>Enzymes</subject><subject>Growth conditions</subject><subject>Insulin</subject><subject>Insulin receptor substrate of 53 kDa (IRSp53)</subject><subject>Lamellipodia</subject><subject>LIN7</subject><subject>Mutants</subject><subject>Mutation</subject><subject>Neurobiology</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Pseudopodia</subject><subject>Rac1 GTPases</subject><subject>Rac1 protein</subject><subject>Research Paper</subject><subject>SOD1 mutants G93A and G147S</subject><subject>Substrates</subject><subject>Superoxide dismutase</subject><subject>Superoxide dismutase 1 (SOD1)</subject><issn>1942-0889</issn><issn>1942-0889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNp9kU1vFSEUhomxsbX6EzSTuHFzbzl8DWxMm_rVpGkX1TVhGKjcMMMVZjT99zLe26Z14QrCec4DnBehN4DXgCU-AcUIllKtCQa5BiaF4OQZOlrOV0vh-aP9IXpZygZjQQnQF-iQYgJMtPgInd5cf4SmTGGYo5lcaaIZXIxhm_pgYrPNacpzCWksTRibKzfn1JCzxlamiWF05RU68CYW93q_HqPvnz99O_-6urz-cnF-drmyjHCyosb6XhLBFcNdJzE3FjhwKqynVAqKMVEdo64njjjDhMGuF4yqTjoFXWvpMbrYeftkNnqbw2DynU4m6L8HKd9qk6dgo9PgXbWBUiAE6w1VhHjbty2IjnXgZXV92Lm2cze43rpxyiY-kT6tjOGHvk2_tABKGKFV8H4vyOnn7Mqkh1CWmZjRpbloAphjqlomKvruH3ST5jzWUVVKKSoYV1ApvqNsTqVk5x8eA1gveev7vPWSt97nXfvePv7JQ9d9wBU43QFh9CkP5nfKsdeTuYsp-2xGG4qm_7_jDwBYt_A</recordid><startdate>20180504</startdate><enddate>20180504</enddate><creator>Ferrari, Ilaria</creator><creator>Verpelli, Chiara</creator><creator>Crespi, Arianna</creator><creator>Sala, Carlo</creator><creator>Fornasari, Diego</creator><creator>Pietrini, Grazia</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7XB</scope><scope>8FD</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-9668-3103</orcidid><orcidid>https://orcid.org/0000-0002-2629-0347</orcidid><orcidid>https://orcid.org/0000-0003-2949-9725</orcidid><orcidid>https://orcid.org/0000-0003-0662-9523</orcidid><orcidid>https://orcid.org/0000-0002-1148-8465</orcidid></search><sort><creationdate>20180504</creationdate><title>SOD1 stimulates lamellipodial protrusions in Neuro 2A cell lines</title><author>Ferrari, Ilaria ; Verpelli, Chiara ; Crespi, Arianna ; Sala, Carlo ; Fornasari, Diego ; Pietrini, Grazia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4252-3acfd8265940bb805ac151536cf338630029b43ed2e2ea46a0ed6439b8e91b7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic lateral Sclerosis (ALS)</topic><topic>Cell differentiation</topic><topic>Cell lines</topic><topic>Cellular biology</topic><topic>Enzymes</topic><topic>Growth conditions</topic><topic>Insulin</topic><topic>Insulin receptor substrate of 53 kDa (IRSp53)</topic><topic>Lamellipodia</topic><topic>LIN7</topic><topic>Mutants</topic><topic>Mutation</topic><topic>Neurobiology</topic><topic>Protein-tyrosine kinase receptors</topic><topic>Pseudopodia</topic><topic>Rac1 GTPases</topic><topic>Rac1 protein</topic><topic>Research Paper</topic><topic>SOD1 mutants G93A and G147S</topic><topic>Substrates</topic><topic>Superoxide dismutase</topic><topic>Superoxide dismutase 1 (SOD1)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ferrari, Ilaria</creatorcontrib><creatorcontrib>Verpelli, Chiara</creatorcontrib><creatorcontrib>Crespi, Arianna</creatorcontrib><creatorcontrib>Sala, Carlo</creatorcontrib><creatorcontrib>Fornasari, Diego</creatorcontrib><creatorcontrib>Pietrini, Grazia</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Technology Research Database</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Communicative & integrative biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ferrari, Ilaria</au><au>Verpelli, Chiara</au><au>Crespi, Arianna</au><au>Sala, Carlo</au><au>Fornasari, Diego</au><au>Pietrini, Grazia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SOD1 stimulates lamellipodial protrusions in Neuro 2A cell lines</atitle><jtitle>Communicative & integrative biology</jtitle><addtitle>Commun Integr Biol</addtitle><date>2018-05-04</date><risdate>2018</risdate><volume>11</volume><issue>3</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>1942-0889</issn><eissn>1942-0889</eissn><abstract>We here investigated the effects of overexpressed superoxide dismutase (SOD)1 and amyotrophic lateral sclerosis (ALS)-linked SOD1 mutants G93A and G147S in Neuro 2A (N2A) cell lines, and found a three-fold increase in lamellipodia either in cells cultured under differentiated or undifferentiated growth conditions. 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| subjects | Amyotrophic lateral sclerosis Amyotrophic lateral Sclerosis (ALS) Cell differentiation Cell lines Cellular biology Enzymes Growth conditions Insulin Insulin receptor substrate of 53 kDa (IRSp53) Lamellipodia LIN7 Mutants Mutation Neurobiology Protein-tyrosine kinase receptors Pseudopodia Rac1 GTPases Rac1 protein Research Paper SOD1 mutants G93A and G147S Substrates Superoxide dismutase Superoxide dismutase 1 (SOD1) |
| title | SOD1 stimulates lamellipodial protrusions in Neuro 2A cell lines |
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