Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells
Identifieur interne : 000031 ( Istex/Corpus ); précédent : 000030; suivant : 000032Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells
Auteurs : Lindsay Marek ; Valerie Levresse ; Claudia Amura ; Eve Zentrich ; Vicki Van Putten ; Raphael A. Nemenoff ; Lynn E. HeasleySource :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2004-12.
English descriptors
- Teeft :
- Activator, Affymetrix, Biol, Biol chem, Cell differentiation, Cell extracts, Chem, Collaborative, Collaborative action, Collapsin response mediator protein, Conduit, Cortexin, Differentiation program, Erks, Extracellular, Extracellular kinase, Gene, Gene expression, Genechip, Global gene expression, Growth factor, Growth factors, Horse serum, Human synapsin, Independent experiments, Induction, Inhibitor, Kinase, Light chain, Mapk, Mapk pathways, Mapks, Marek, Mrna, Multiple signal conduits, Muscle cells, Nerve growth factor, Neural differentiation, Neuronal, Neuronal differentiation, Nflc, Nflc promoter, Pathway, Pheochromocytoma cells, Plasminogen, Previous study, Primer, Proc natl acad, Promoter, Protein kinase, Receptor, Signal conduit, Signal conduits, Synapsin, Synapsin reporter, Tgfb1, Transcription, Transcriptional, Transcriptional regulation, Transfected, Transfected cells, Upar, Urokinase plasminogen activator receptor, Zentrich.
Abstract
PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jcp.20087
Links to Exploration step
ISTEX:02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000Le document en format XML
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We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. 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Nemenoff</name><affiliations><json:string>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</json:string></affiliations></json:item><json:item><name>Lynn E. Heasley</name><affiliations><json:string>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</json:string><json:string>Division of Renal Medicine, C‐281, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262.</json:string></affiliations></json:item></author><articleId><json:string>JCP20087</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>592 x 789 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>2114</abstractCharCount><pdfWordCount>6875</pdfWordCount><pdfCharCount>46183</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>285</abstractWordCount></qualityIndicators><title>Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title><genre><json:string>article</json:string></genre><host><title>Journal of Cellular Physiology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1097-4652</json:string></doi><issn><json:string>0021-9541</json:string></issn><eissn><json:string>1097-4652</json:string></eissn><publisherId><json:string>JCP</json:string></publisherId><volume>201</volume><issue>3</issue><pages><first>459</first><last>469</last><total>11</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Article</value></json:item></subject></host><categories><wos><json:string>science</json:string><json:string>physiology</json:string><json:string>cell biology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>biochemistry & molecular biology</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences biologiques fondamentales et appliquees. psychologie</json:string><json:string>genetique des eucaryotes. evolution biologique et moleculaire</json:string></inist></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1002/jcp.20087</json:string></doi><id>02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 2004 Wiley‐Liss, Inc.</p></availability><date>2004</date></publicationStmt><notesStmt><note>National Institutes of Health - No. GM61718; No. DK59756;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title><author xml:id="author-1"><persName><forename type="first">Lindsay</forename><surname>Marek</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-2"><persName><forename type="first">Valerie</forename><surname>Levresse</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-3"><persName><forename type="first">Claudia</forename><surname>Amura</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-4"><persName><forename type="first">Eve</forename><surname>Zentrich</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-5"><persName><forename type="first">Vicki Van</forename><surname>Putten</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-6"><persName><forename type="first">Raphael A.</forename><surname>Nemenoff</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation></author><author xml:id="author-7"><persName><forename type="first">Lynn E.</forename><surname>Heasley</surname></persName><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><affiliation>Division of Renal Medicine, C‐281, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262.</affiliation></author></analytic><monogr><title level="j">Journal of Cellular Physiology</title><title level="j" type="abbrev">J. Cell. Physiol.</title><idno type="pISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><idno type="DOI">10.1002/(ISSN)1097-4652</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-12"></date><biblScope unit="volume">201</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="459">459</biblScope><biblScope unit="page" to="469">469</biblScope></imprint></monogr><idno type="istex">02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000</idno><idno type="DOI">10.1002/jcp.20087</idno><idno type="ArticleID">JCP20087</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-01-29">Received</change><change when="2004-02-09">Registration</change><change when="2004-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4652</doi><issn type="print">0021-9541</issn><issn type="electronic">1097-4652</issn><idGroup><id type="product" value="JCP"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR PHYSIOLOGY">Journal of Cellular Physiology</title><title type="short">J. Cell. Physiol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/jcp.v201:3</doi><numberingGroup><numbering type="journalVolume" number="201">201</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2004-12">December 2004</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="150" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcp.20087</doi><idGroup><id type="unit" value="JCP20087"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2004 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2004-01-29"></event><event type="manuscriptAccepted" date="2004-02-09"></event><event type="publishedOnlineEarlyUnpaginated" date="2004-06-01"></event><event type="firstOnline" date="2004-06-01"></event><event type="publishedOnlineFinalForm" date="2004-09-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-05"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">459</numbering><numbering type="pageLast">469</numbering></numberingGroup><correspondenceTo>Division of Renal Medicine, C‐281, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCP.JCP20087.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="49"></count><count type="wordTotal" number="8401"></count></countGroup><titleGroup><title type="main" xml:lang="en">Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title><title type="short" xml:lang="en">MULTIPLE SIGNAL CONDUITS IN PC12 CELL DIFFERENTIATION</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Lindsay</givenNames><familyName>Marek</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Valerie</givenNames><familyName>Levresse</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Claudia</givenNames><familyName>Amura</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Eve</givenNames><familyName>Zentrich</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Vicki Van</givenNames><familyName>Putten</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Raphael A.</givenNames><familyName>Nemenoff</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Lynn E.</givenNames><familyName>Heasley</familyName></personName><contactDetails><email>Lynn.Heasley@UCHSC.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>GM61718</fundingNumber><fundingNumber>DK59756</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (<i>NFLC</i>) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (<i>NFLC</i>, <i>transin</i>, <i>uPAR</i>) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MULTIPLE SIGNAL CONDUITS IN PC12 CELL DIFFERENTIATION</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Multiple signaling conduits regulate global differentiation‐specific gene expression in PC12 cells</title></titleInfo><name type="personal"><namePart type="given">Lindsay</namePart><namePart type="family">Marek</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Valerie</namePart><namePart type="family">Levresse</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Amura</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eve</namePart><namePart type="family">Zentrich</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vicki Van</namePart><namePart type="family">Putten</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raphael A.</namePart><namePart type="family">Nemenoff</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lynn E.</namePart><namePart type="family">Heasley</namePart><affiliation>Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado</affiliation><affiliation>Division of Renal Medicine, C‐281, University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2004-12</dateIssued><dateCaptured encoding="w3cdtf">2004-01-29</dateCaptured><dateValid encoding="w3cdtf">2004-02-09</dateValid><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">6</extent><extent unit="tables">3</extent><extent unit="references">49</extent><extent unit="words">8401</extent></physicalDescription><abstract lang="en">PC12 cells serve as a model for exploring nerve growth factor (NGF)‐stimulated signal pathways that mediate neural differentiation. We previously demonstrated that neurofilament light chain (NFLC) gene induction by NGF requires collaborative extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) signaling. Herein, we investigate the broader requirement for integrated ERK and JNK signaling in NGF‐stimulated gene expression. NGF stimulates differentiation as well as maintenance of cell viability while insulin‐like growth factor‐1 (IGF‐1) stimulates only trophic actions in PC12 cells. Affymetrix Genechips were used to identify genes whose expression specifically increased in response to NGF, but not IGF‐1. From the set of NGF‐specific genes, the induction by NGF of ten genes with diverse predicted cellular functions was tested for ERK and JNK pathway requirements using the protein kinase inhibitors, PD98059 and SP600125, respectively. Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra‐1 and transforming growth factor β1 (TGFβ1) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 (rCRMP4), rat growth and transformation‐dependent protein (RGT), and synapsin II required neither mitogen‐activated protein kinase (MAPK) pathway. NGF‐induction of the bradykinin B2 receptor and c‐Ret mRNAs was partially inhibited by SP600125, but not PD98059. Reporter constructs containing the promoters for ERK/JNK‐dependent genes (NFLC, transin, uPAR) as well as an ERK/JNK‐independent gene (synapsin II) revealed that both sets of genes required functional Ras signaling for activation by NGF. Integrated signaling through the ERK and JNK MAPKs, therefore, represents a general conduit for NGF‐dependent gene expression, but additional Ras‐dependent signaling pathways distinct from the ERKs and JNKs must contribute as well. Thus, multiple signaling conduits control global differentiation‐specific gene expression in PC12 cells. © 2004 Wiley‐Liss, Inc.</abstract><note type="funding">National Institutes of Health - No. GM61718; No. DK59756; </note><relatedItem type="host"><titleInfo><title>Journal of Cellular Physiology</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. Physiol.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0021-9541</identifier><identifier type="eISSN">1097-4652</identifier><identifier type="DOI">10.1002/(ISSN)1097-4652</identifier><identifier type="PublisherID">JCP</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>201</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>459</start><end>469</end><total>11</total></extent></part></relatedItem><identifier type="istex">02DDA9AC51ECDAE36D1FA98A7BACFCCE2C424000</identifier><identifier type="DOI">10.1002/jcp.20087</identifier><identifier type="ArticleID">JCP20087</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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