Inhibition of Alanyl-Aminopeptidase Suppresses the Activation-Dependent Induction of Glycogen Synthase Kinase-3β (GSK-3β) in Human T Cells
Identifieur interne : 000434 ( Istex/Corpus ); précédent : 000433; suivant : 000435Inhibition of Alanyl-Aminopeptidase Suppresses the Activation-Dependent Induction of Glycogen Synthase Kinase-3β (GSK-3β) in Human T Cells
Auteurs : Uwe Lendeckel ; Beate Scholz ; Marco Arndt ; Karin Frank ; Antje Spiess ; Huixiong Chen ; Bernard P. Roques ; Siegfried AnsorgeSource :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 2000.
English descriptors
- KwdEn :
- Teeft :
- Academic press, Actinonin, Alanyl aminopeptidase, Aminopeptidase, Aminopeptidase inhibitors, Ansorge, Arndt, Biophysical research communications, Cell activation, Cell growth, Cell proliferation, Culture medium, England biolabs, Febs lett, Glycogen synthase, Idaho technology, Inhibitor, Lendeckel, Mrna, Mrna amounts, Mrna content, Pokeweed mitogen, Protein amounts, Quantitative determination, Strong increase, Trends genet, Upstate biotechnology.
Abstract
Abstract: Inhibition of alanyl-aminopeptidase (APN, CD13) gene expression or enzymatic activity compromises T cell proliferation and function. Molecular mechanisms mediating these effects are not known as yet. Recently, we found the expression of the proto-oncogen Wnt-5a to be strongly affected by APN-inhibition. Wnt-5a and other members of the Wnt family of secreted factors are implicated in cell growth and differentiation. Here, we analyzed by quantitative RT-PCR and immunoblotting the expression in mitogen-activated T cells of a major constituent of the Wnt-5a pathway, glycogen synthase kinase-3β (GSK-3β). T cell activation by phytohaemagglutinin or pokeweed mitogen results in a strong increase of GSK-3β mRNA amounts. At the protein level, we observed an up-regulation of both GSK-3β and phosphorylated GSK-3β. This induction-dependent increase of GSK-3β is markedly reduced in response to inhibitors of alanyl-aminopeptidase, actinonin, leuhistin, and RB3014. These findings may provide a rational for the growth inhibition resulting from a diminished expression or activity of alanyl aminopeptidase.
Url:
DOI: 10.1006/bbrc.2000.2883
Links to Exploration step
ISTEX:72C5A439E086ADA4F61577B3086BB5C8812B0645Le document en format XML
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Clin</json:string><json:string>Karin Frank</json:string><json:string>Christine Wolf</json:string></persName><placeName><json:string>Germany</json:string><json:string>Nakashima</json:string><json:string>Magdeburg</json:string><json:string>Morioka</json:string></placeName><ref_url><json:string>http://www.idealibrary.com</json:string></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[45]</json:string><json:string>[33]</json:string><json:string>[43, 44]</json:string><json:string>[28]</json:string><json:string>[21]</json:string><json:string>[27]</json:string><json:string>[2, 3]</json:string><json:string>[5]</json:string><json:string>[37]</json:string><json:string>[30]</json:string><json:string>[36]</json:string><json:string>[31, 32]</json:string><json:string>Thomas et al. [40]</json:string><json:string>[46]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-HVS7QP6T-G</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - biophysics</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cell Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - 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Internal Medicine</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Beate</forename><surname>Scholz</surname></persName><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Marco</forename><surname>Arndt</surname></persName><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Karin</forename><surname>Frank</surname></persName><affiliation>Institute of Experimental Internal Medicine, Center of Internal Medicine</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Antje</forename><surname>Spiess</surname></persName><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Huixiong</forename><surname>Chen</surname></persName><affiliation>Département de Pharmacochimie Moléculaire et Structurale INSERM U266- CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, 4, avenue de l′Observatoire, 75270, Paris Cedex 06, France</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Bernard P.</forename><surname>Roques</surname></persName><affiliation>Département de Pharmacochimie Moléculaire et Structurale INSERM U266- CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, 4, avenue de l′Observatoire, 75270, Paris Cedex 06, France</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Siegfried</forename><surname>Ansorge</surname></persName><affiliation>Institute of Experimental Internal Medicine, Center of Internal Medicine</affiliation></author><idno type="istex">72C5A439E086ADA4F61577B3086BB5C8812B0645</idno><idno type="ark">ark:/67375/6H6-HVS7QP6T-G</idno><idno type="DOI">10.1006/bbrc.2000.2883</idno><idno type="PII">S0006-291X(00)92883-3</idno><idno type="article-id">92883</idno></analytic><monogr><title level="j">Biochemical and Biophysical Research Communications</title><title level="j" type="abbrev">YBBRC</title><idno type="pISSN">0006-291X</idno><idno type="PII">S0006-291X(00)X0048-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">273</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="62">62</biblScope><biblScope unit="page" to="65">65</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Inhibition of alanyl-aminopeptidase (APN, CD13) gene expression or enzymatic activity compromises T cell proliferation and function. Molecular mechanisms mediating these effects are not known as yet. Recently, we found the expression of the proto-oncogen Wnt-5a to be strongly affected by APN-inhibition. Wnt-5a and other members of the Wnt family of secreted factors are implicated in cell growth and differentiation. Here, we analyzed by quantitative RT-PCR and immunoblotting the expression in mitogen-activated T cells of a major constituent of the Wnt-5a pathway, glycogen synthase kinase-3β (GSK-3β). T cell activation by phytohaemagglutinin or pokeweed mitogen results in a strong increase of GSK-3β mRNA amounts. At the protein level, we observed an up-regulation of both GSK-3β and phosphorylated GSK-3β. This induction-dependent increase of GSK-3β is markedly reduced in response to inhibitors of alanyl-aminopeptidase, actinonin, leuhistin, and RB3014. These findings may provide a rational for the growth inhibition resulting from a diminished expression or activity of alanyl aminopeptidase.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>alanyl aminopeptidase</term></item><item><term>CD13</term></item><item><term>cell proliferation</term></item><item><term>Wnt-5a</term></item><item><term>GSK-3β</term></item><item><term>quantitative PCR</term></item><item><term>Lightcycler</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-HVS7QP6T-G/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YBBRC</jid><aid>92883</aid><ce:pii>S0006-291X(00)92883-3</ce:pii><ce:doi>10.1006/bbrc.2000.2883</ce:doi><ce:copyright type="full-transfer" year="2000">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Inhibition of Alanyl-Aminopeptidase Suppresses the Activation-Dependent Induction of Glycogen Synthase Kinase-3β (GSK-3β) in Human T Cells</ce:title><ce:author-group><ce:author><ce:given-name>Uwe</ce:given-name><ce:surname>Lendeckel</ce:surname><ce:cross-ref refid="A0"><ce:sup loc="post">a</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Beate</ce:given-name><ce:surname>Scholz</ce:surname><ce:cross-ref refid="A1"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Marco</ce:given-name><ce:surname>Arndt</ce:surname><ce:cross-ref refid="A1"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Karin</ce:given-name><ce:surname>Frank</ce:surname><ce:cross-ref refid="A0"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Antje</ce:given-name><ce:surname>Spiess</ce:surname><ce:cross-ref refid="A1"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Huixiong</ce:given-name><ce:surname>Chen</ce:surname><ce:cross-ref refid="A2"><ce:sup loc="post">c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Bernard P.</ce:given-name><ce:surname>Roques</ce:surname><ce:cross-ref refid="A2"><ce:sup loc="post">c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Siegfried</ce:given-name><ce:surname>Ansorge</ce:surname><ce:cross-ref refid="A0"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="A0"><ce:label>a</ce:label><ce:textfn>Institute of Experimental Internal Medicine, Center of Internal Medicine</ce:textfn></ce:affiliation><ce:affiliation id="A1"><ce:label>b</ce:label><ce:textfn>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</ce:textfn></ce:affiliation><ce:affiliation id="A2"><ce:label>c</ce:label><ce:textfn>Département de Pharmacochimie Moléculaire et Structurale INSERM U266- CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, 4, avenue de l′Observatoire, 75270, Paris Cedex 06, France</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>To whom correspondence should be addressed. Fax: (49) 0391 67190130. E-mail: uwe.lendeckel@medizin.uni-magdeburg.de.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="14" month="5" year="2000"></ce:date-received><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Inhibition of alanyl-aminopeptidase (APN, CD13) gene expression or enzymatic activity compromises T cell proliferation and function. Molecular mechanisms mediating these effects are not known as yet. Recently, we found the expression of the proto-oncogen Wnt-5a to be strongly affected by APN-inhibition. Wnt-5a and other members of the Wnt family of secreted factors are implicated in cell growth and differentiation. Here, we analyzed by quantitative RT-PCR and immunoblotting the expression in mitogen-activated T cells of a major constituent of the Wnt-5a pathway, glycogen synthase kinase-3β (GSK-3β). T cell activation by phytohaemagglutinin or pokeweed mitogen results in a strong increase of GSK-3β mRNA amounts. At the protein level, we observed an up-regulation of both GSK-3β and phosphorylated GSK-3β. This induction-dependent increase of GSK-3β is markedly reduced in response to inhibitors of alanyl-aminopeptidase, actinonin, leuhistin, and RB3014. These findings may provide a rational for the growth inhibition resulting from a diminished expression or activity of alanyl aminopeptidase.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>alanyl aminopeptidase</ce:text></ce:keyword><ce:keyword><ce:text>CD13</ce:text></ce:keyword><ce:keyword><ce:text>cell proliferation</ce:text></ce:keyword><ce:keyword><ce:text>Wnt-5a</ce:text></ce:keyword><ce:keyword><ce:text>GSK-3β</ce:text></ce:keyword><ce:keyword><ce:text>quantitative PCR</ce:text></ce:keyword><ce:keyword><ce:text>Lightcycler</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Inhibition of Alanyl-Aminopeptidase Suppresses the Activation-Dependent Induction of Glycogen Synthase Kinase-3β (GSK-3β) in Human T Cells</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Inhibition of Alanyl-Aminopeptidase Suppresses the Activation-Dependent Induction of Glycogen Synthase Kinase-3β (GSK-3β) in Human T Cells</title></titleInfo><name type="personal"><namePart type="given">Uwe</namePart><namePart type="family">Lendeckel</namePart><affiliation>Institute of Experimental Internal Medicine, Center of Internal Medicine</affiliation><description>To whom correspondence should be addressed. Fax: (49) 0391 67190130. E-mail: uwe.lendeckel@medizin.uni-magdeburg.de.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Beate</namePart><namePart type="family">Scholz</namePart><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marco</namePart><namePart type="family">Arndt</namePart><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karin</namePart><namePart type="family">Frank</namePart><affiliation>Institute of Experimental Internal Medicine, Center of Internal Medicine</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antje</namePart><namePart type="family">Spiess</namePart><affiliation>Institute of Immunology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120, Magdeburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Huixiong</namePart><namePart type="family">Chen</namePart><affiliation>Département de Pharmacochimie Moléculaire et Structurale INSERM U266- CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, 4, avenue de l′Observatoire, 75270, Paris Cedex 06, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bernard P.</namePart><namePart type="family">Roques</namePart><affiliation>Département de Pharmacochimie Moléculaire et Structurale INSERM U266- CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, 4, avenue de l′Observatoire, 75270, Paris Cedex 06, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Siegfried</namePart><namePart type="family">Ansorge</namePart><affiliation>Institute of Experimental Internal Medicine, Center of Internal Medicine</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Inhibition of alanyl-aminopeptidase (APN, CD13) gene expression or enzymatic activity compromises T cell proliferation and function. Molecular mechanisms mediating these effects are not known as yet. Recently, we found the expression of the proto-oncogen Wnt-5a to be strongly affected by APN-inhibition. Wnt-5a and other members of the Wnt family of secreted factors are implicated in cell growth and differentiation. Here, we analyzed by quantitative RT-PCR and immunoblotting the expression in mitogen-activated T cells of a major constituent of the Wnt-5a pathway, glycogen synthase kinase-3β (GSK-3β). T cell activation by phytohaemagglutinin or pokeweed mitogen results in a strong increase of GSK-3β mRNA amounts. At the protein level, we observed an up-regulation of both GSK-3β and phosphorylated GSK-3β. This induction-dependent increase of GSK-3β is markedly reduced in response to inhibitors of alanyl-aminopeptidase, actinonin, leuhistin, and RB3014. These findings may provide a rational for the growth inhibition resulting from a diminished expression or activity of alanyl aminopeptidase.</abstract><note type="content">Section title: Regular Article</note><subject lang="en"><genre>Keywords</genre><topic>alanyl aminopeptidase</topic><topic>CD13</topic><topic>cell proliferation</topic><topic>Wnt-5a</topic><topic>GSK-3β</topic><topic>quantitative PCR</topic><topic>Lightcycler</topic></subject><relatedItem type="host"><titleInfo><title>Biochemical and Biophysical Research Communications</title></titleInfo><titleInfo type="abbreviated"><title>YBBRC</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued></originInfo><identifier type="ISSN">0006-291X</identifier><identifier type="PII">S0006-291X(00)X0048-4</identifier><part><date>2000</date><detail type="volume"><number>273</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>391</end></extent><extent unit="pages"><start>62</start><end>65</end></extent></part></relatedItem><identifier type="istex">72C5A439E086ADA4F61577B3086BB5C8812B0645</identifier><identifier type="ark">ark:/67375/6H6-HVS7QP6T-G</identifier><identifier type="DOI">10.1006/bbrc.2000.2883</identifier><identifier type="PII">S0006-291X(00)92883-3</identifier><identifier type="ArticleID">92883</identifier><accessCondition type="use and reproduction" contentType="copyright">©2000 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©2000</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-HVS7QP6T-G/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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