Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16
Identifieur interne : 002764 ( Istex/Corpus ); précédent : 002763; suivant : 002765Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16
Auteurs : Catherine Damien ; Patrick Robberecht ; Robert Hooghe ; Philippe De Neef ; Jean ChristopheSource :
- Peptides [ 0196-9781 ] ; 1989.
English descriptors
- Teeft :
- Adenylate, Adenylate cyclase, Adenylate cyclase activation, Adenylate cyclase activity, Adenylate cyclase system, Cell line, Cell lines, Cell membranes, Cholera, Cholera toxin, Christophe, Clone, Cyclase, Cyclic, Febs lett, Helodermin, Higher potency, Melanoma, Melanoma cells, Melanoma clones, Membrane, Mouse melanoma, Mouse melanoma cell line, Neef, Peptide, Pmol cyclic, Prostaglandin, Receptor, Robberecht, Toxin.
Abstract
Abstract: We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His1]VIP, and also by PGE1. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE1 were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE1 receptors.
Url:
DOI: 10.1016/0196-9781(89)90192-7
Links to Exploration step
ISTEX:DA95B6813B99D583FE43603232D1898B3A18E72FLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title><author><name sortKey="Damien, Catherine" sort="Damien, Catherine" uniqKey="Damien C" first="Catherine" last="Damien">Catherine Damien</name><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Robberecht, Patrick" sort="Robberecht, Patrick" uniqKey="Robberecht P" first="Patrick" last="Robberecht">Patrick Robberecht</name></author><author><name sortKey="Hooghe, Robert" sort="Hooghe, Robert" uniqKey="Hooghe R" first="Robert" last="Hooghe">Robert Hooghe</name><affiliation><mods:affiliation>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</mods:affiliation></affiliation></author><author><name sortKey="De Neef, Philippe" sort="De Neef, Philippe" uniqKey="De Neef P" first="Philippe" last="De Neef">Philippe De Neef</name><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Christophe, Jean" sort="Christophe, Jean" uniqKey="Christophe J" first="Jean" last="Christophe">Jean Christophe</name><affiliation><mods:affiliation>Requests for reprints should be addressed to Jean Christophe.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DA95B6813B99D583FE43603232D1898B3A18E72F</idno><date when="1989" year="1989">1989</date><idno type="doi">10.1016/0196-9781(89)90192-7</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-202G12D1-V/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002764</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002764</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title><author><name sortKey="Damien, Catherine" sort="Damien, Catherine" uniqKey="Damien C" first="Catherine" last="Damien">Catherine Damien</name><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Robberecht, Patrick" sort="Robberecht, Patrick" uniqKey="Robberecht P" first="Patrick" last="Robberecht">Patrick Robberecht</name></author><author><name sortKey="Hooghe, Robert" sort="Hooghe, Robert" uniqKey="Hooghe R" first="Robert" last="Hooghe">Robert Hooghe</name><affiliation><mods:affiliation>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</mods:affiliation></affiliation></author><author><name sortKey="De Neef, Philippe" sort="De Neef, Philippe" uniqKey="De Neef P" first="Philippe" last="De Neef">Philippe De Neef</name><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author><author><name sortKey="Christophe, Jean" sort="Christophe, Jean" uniqKey="Christophe J" first="Jean" last="Christophe">Jean Christophe</name><affiliation><mods:affiliation>Requests for reprints should be addressed to Jean Christophe.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Peptides</title><title level="j" type="abbrev">PEP</title><idno type="ISSN">0196-9781</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989">1989</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1075">1075</biblScope><biblScope unit="page" to="1079">1079</biblScope></imprint><idno type="ISSN">0196-9781</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0196-9781</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adenylate</term><term>Adenylate cyclase</term><term>Adenylate cyclase activation</term><term>Adenylate cyclase activity</term><term>Adenylate cyclase system</term><term>Cell line</term><term>Cell lines</term><term>Cell membranes</term><term>Cholera</term><term>Cholera toxin</term><term>Christophe</term><term>Clone</term><term>Cyclase</term><term>Cyclic</term><term>Febs lett</term><term>Helodermin</term><term>Higher potency</term><term>Melanoma</term><term>Melanoma cells</term><term>Melanoma clones</term><term>Membrane</term><term>Mouse melanoma</term><term>Mouse melanoma cell line</term><term>Neef</term><term>Peptide</term><term>Pmol cyclic</term><term>Prostaglandin</term><term>Receptor</term><term>Robberecht</term><term>Toxin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His1]VIP, and also by PGE1. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE1 were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE1 receptors.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>cyclase</json:string><json:string>adenylate</json:string><json:string>receptor</json:string><json:string>melanoma</json:string><json:string>helodermin</json:string><json:string>clone</json:string><json:string>adenylate cyclase activity</json:string><json:string>robberecht</json:string><json:string>christophe</json:string><json:string>peptide</json:string><json:string>neef</json:string><json:string>cyclic</json:string><json:string>cell lines</json:string><json:string>adenylate cyclase</json:string><json:string>cholera toxin</json:string><json:string>prostaglandin</json:string><json:string>toxin</json:string><json:string>cell membranes</json:string><json:string>cholera</json:string><json:string>febs lett</json:string><json:string>higher potency</json:string><json:string>adenylate cyclase activation</json:string><json:string>mouse melanoma cell line</json:string><json:string>melanoma cells</json:string><json:string>pmol cyclic</json:string><json:string>cell line</json:string><json:string>mouse melanoma</json:string><json:string>adenylate cyclase system</json:string><json:string>melanoma clones</json:string><json:string>membrane</json:string></teeft></keywords><author><json:item><name>Catherine Damien</name><affiliations><json:string>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</json:string></affiliations></json:item><json:item><name>Patrick Robberecht</name></json:item><json:item><name>Robert Hooghe</name><affiliations><json:string>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</json:string></affiliations></json:item><json:item><name>Philippe De Neef</name><affiliations><json:string>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</json:string></affiliations></json:item><json:item><name>Jean Christophe</name><affiliations><json:string>Requests for reprints should be addressed to Jean Christophe.</json:string><json:string>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Mouse melanoma cells B16</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>VIP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Helodermin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>α-MSH</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Prostaglandin E1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Adenylate cyclase</value></json:item></subject><arkIstex>ark:/67375/6H6-202G12D1-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His1]VIP, and also by PGE1. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE1 were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE1 receptors.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>150</abstractWordCount><abstractCharCount>1010</abstractCharCount><keywordCount>6</keywordCount><score>6.795</score><pdfWordCount>2995</pdfWordCount><pdfCharCount>18488</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>598 x 792 pts</pdfPageSize></qualityIndicators><title>Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title><pmid><json:string>2558362</json:string></pmid><pii><json:string>0196-9781(89)90192-7</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. USA</title><language><json:string>unknown</json:string></language><volume>75</volume><pages><first>3050</first><last>3054</last></pages></serie><host><title>Peptides</title><language><json:string>unknown</json:string></language><publicationDate>1989</publicationDate><issn><json:string>0196-9781</json:string></issn><pii><json:string>S0196-9781(00)X0151-9</json:string></pii><volume>10</volume><issue>5</issue><pages><first>1075</first><last>1079</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1989</json:string></date><geogName></geogName><orgName><json:string>Tulane University</json:string><json:string>Novabiochem</json:string><json:string>Commission of the European Communities</json:string><json:string>Medical Scientific Research</json:string><json:string>Behring Co.</json:string><json:string>Sigma Chemical Co.</json:string><json:string>Grant STJ-001</json:string></orgName><orgName_funder><json:string>Grant STJ-001</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>I. Helodermin</json:string><json:string>Jean Christophe</json:string><json:string>D. H. Coy</json:string><json:string>La Jolla</json:string><json:string>Friedrich Miescher</json:string></persName><placeName><json:string>Switzerland</json:string><json:string>Mannheim</json:string><json:string>LA</json:string><json:string>New Orleans</json:string><json:string>MO</json:string><json:string>Europe</json:string><json:string>Basel</json:string><json:string>St Louis</json:string><json:string>Belgium</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Luis et al.</json:string><json:string>Gerst et al.</json:string><json:string>Salomon et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-202G12D1-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - pharmacology & pharmacy</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - endocrinology & metabolism</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Cellular and Molecular Neuroscience</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Endocrinology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Physiology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Biochemistry</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string><json:string>4 - embryologie: invertebres et vertebres. teratologie</json:string></inist></categories><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1016/0196-9781(89)90192-7</json:string></doi><id>DA95B6813B99D583FE43603232D1898B3A18E72F</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-202G12D1-V/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-202G12D1-V/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-202G12D1-V/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1989</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title><author xml:id="author-0000"><persName><forename type="first">Catherine</forename><surname>Damien</surname></persName><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Patrick</forename><surname>Robberecht</surname></persName></author><author xml:id="author-0002"><persName><forename type="first">Robert</forename><surname>Hooghe</surname></persName><affiliation>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Philippe</forename><surname>De Neef</surname></persName><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Jean</forename><surname>Christophe</surname></persName><affiliation>Requests for reprints should be addressed to Jean Christophe.</affiliation><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</affiliation></author><idno type="istex">DA95B6813B99D583FE43603232D1898B3A18E72F</idno><idno type="ark">ark:/67375/6H6-202G12D1-V</idno><idno type="DOI">10.1016/0196-9781(89)90192-7</idno><idno type="PII">0196-9781(89)90192-7</idno></analytic><monogr><title level="j">Peptides</title><title level="j" type="abbrev">PEP</title><idno type="pISSN">0196-9781</idno><idno type="PII">S0196-9781(00)X0151-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989"></date><biblScope unit="volume">10</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1075">1075</biblScope><biblScope unit="page" to="1079">1079</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1989</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His1]VIP, and also by PGE1. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE1 were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE1 receptors.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Mouse melanoma cells B16</term></item><item><term>VIP</term></item><item><term>Helodermin</term></item><item><term>α-MSH</term></item><item><term>Prostaglandin E1</term></item><item><term>Adenylate cyclase</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-202G12D1-V/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"><item-info><jid>PEP</jid><aid>89901927</aid><ce:pii>0196-9781(89)90192-7</ce:pii><ce:doi>10.1016/0196-9781(89)90192-7</ce:doi><ce:copyright type="unknown" year="1989"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Decreased adenylate cyclase activation by helodermin and PGE<ce:inf>1</ce:inf> in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</ce:title><ce:author-group><ce:author><ce:given-name>Catherine</ce:given-name><ce:surname>Damien</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Patrick</ce:given-name><ce:surname>Robberecht</ce:surname></ce:author><ce:author><ce:given-name>Robert</ce:given-name><ce:surname>Hooghe</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Philippe</ce:given-name><ce:surname>De Neef</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jean</ce:given-name><ce:surname>Christophe</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Requests for reprints should be addressed to Jean Christophe.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="20" month="3" year="1989"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His<ce:sup>1</ce:sup>]VIP, and also by PGE<ce:inf>1</ce:inf>. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE<ce:inf>1</ce:inf> were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE<ce:inf>1</ce:inf> receptors.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Mouse melanoma cells B16</ce:text></ce:keyword><ce:keyword><ce:text>VIP</ce:text></ce:keyword><ce:keyword><ce:text>Helodermin</ce:text></ce:keyword><ce:keyword><ce:text>α-MSH</ce:text></ce:keyword><ce:keyword><ce:text>Prostaglandin E<ce:inf>1</ce:inf></ce:text></ce:keyword><ce:keyword><ce:text>Adenylate cyclase</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Decreased adenylate cyclase activation by helodermin and PGE</title></titleInfo><name type="personal"><namePart type="given">Catherine</namePart><namePart type="family">Damien</namePart><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrick</namePart><namePart type="family">Robberecht</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert</namePart><namePart type="family">Hooghe</namePart><affiliation>Department of Radiobiology, SCK-CEN, B-2400 Mol, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">De Neef</namePart><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean</namePart><namePart type="family">Christophe</namePart><affiliation>Requests for reprints should be addressed to Jean Christophe.</affiliation><affiliation>Department of Biochemistry and Nutrition, Medical School, Université Libre de Bruxelles Boulevard de Waterloo 115, B-1000 Brussels, Belgium</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">1989</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: We examined the cultured mouse melanoma cell line B16 (clone F1) and its wheat germ agglutinin-resistant variant Wa4 that suffers from abnormal protein glycosylation (a high fucose:sialic acid ratio in glycoproteins). In both cell lines the adenylate cyclase system was endowed with a functional guanine nucleotide binding protein Gs and was efficiently coupled to α-MSH receptors. In the B16 cell line F1 studied we also observed an efficient stimulation of adenylate cyclase activity by helodermin, VIP and the VIP analogue [acetyl-His1]VIP, and also by PGE1. In membranes from the lectin-resistant variant Wa4, the stimulations by VIP-like peptides and by PGE1 were reduced by 60% and 50%, respectively, while the stimulation by α-MSH remained normal. As other components of the adenylate cyclase system (Gs site, catalytical unit) appeared unchanged in the Wa4 variant, we conclude that impaired glycosylation essentially affected the number of both VIP-like peptide receptors and PGE1 receptors.</abstract><note type="content">Section title: Article</note><subject><genre>Keywords</genre><topic>Mouse melanoma cells B16</topic><topic>VIP</topic><topic>Helodermin</topic><topic>α-MSH</topic><topic>Prostaglandin E1</topic><topic>Adenylate cyclase</topic></subject><relatedItem type="host"><titleInfo><title>Peptides</title></titleInfo><titleInfo type="abbreviated"><title>PEP</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">1989</dateIssued></originInfo><identifier type="ISSN">0196-9781</identifier><identifier type="PII">S0196-9781(00)X0151-9</identifier><part><date>1989</date><detail type="volume"><number>10</number><caption>vol.</caption></detail><detail type="issue"><number>5</number><caption>no.</caption></detail><extent unit="issue-pages"><start>903</start><end>1115</end></extent><extent unit="pages"><start>1075</start><end>1079</end></extent></part></relatedItem><identifier type="istex">DA95B6813B99D583FE43603232D1898B3A18E72F</identifier><identifier type="ark">ark:/67375/6H6-202G12D1-V</identifier><identifier type="DOI">10.1016/0196-9781(89)90192-7</identifier><identifier type="PII">0196-9781(89)90192-7</identifier><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></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-202G12D1-V/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002764 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 002764 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:DA95B6813B99D583FE43603232D1898B3A18E72F
|texte= Decreased adenylate cyclase activation by helodermin and PGE1 in the lectin-resistant variant Wa4 of the mouse melanoma cell line B16
}}
| This area was generated with Dilib version V0.6.33. |  |