Generation and characterization of a constitutively active Stat3 protein
Identifieur interne : 001106 ( Istex/Corpus ); précédent : 001105; suivant : 001107Generation and characterization of a constitutively active Stat3 protein
Auteurs : Juan A. Barboza ; Shuguang Wang ; Timothy S. SchaeferSource :
- Molecular Biology Reports [ 0301-4851 ] ; 2004-03-01.
English descriptors
Abstract
Abstract: Stats are latent transcription factors involved in normal cellular signaling in response to cytokine or growth factor stimulation. Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (VP16 activation domain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c-myc and c-fos genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.
Url:
DOI: 10.1023/B:MOLE.0000013503.16301.82
Links to Exploration step
ISTEX:19514631FEA48FE7D9822F872ED4A4EACD22306CLe document en format XML
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Barboza</name><affiliation><mods:affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</mods:affiliation></affiliation></author><author><name sortKey="Wang, Shuguang" sort="Wang, Shuguang" uniqKey="Wang S" first="Shuguang" last="Wang">Shuguang Wang</name><affiliation><mods:affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</mods:affiliation></affiliation></author><author><name sortKey="Schaefer, Timothy S" sort="Schaefer, Timothy S" uniqKey="Schaefer T" first="Timothy S." last="Schaefer">Timothy S. Schaefer</name><affiliation><mods:affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Molecular Biology Reports</title><title level="j" type="sub">An International Journal on Molecular and Cellular Biology</title><title level="j" type="abbrev">Mol Biol Rep</title><idno type="ISSN">0301-4851</idno><idno type="eISSN">1573-4978</idno><imprint><publisher>Kluwer Academic Publishers</publisher><pubPlace>Dordrecht</pubPlace><date type="published" when="2004-03-01">2004-03-01</date><biblScope unit="volume">31</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="13">13</biblScope><biblScope unit="page" to="21">21</biblScope></imprint><idno type="ISSN">0301-4851</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0301-4851</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>oncogene</term><term>phosphoprotein</term><term>signal transduction</term><term>transcription factor</term><term>tyrosine kinase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Stats are latent transcription factors involved in normal cellular signaling in response to cytokine or growth factor stimulation. Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (VP16 activation domain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c-myc and c-fos genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Juan A. Barboza</name><affiliations><json:string>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</json:string></affiliations></json:item><json:item><name>Shuguang Wang</name><affiliations><json:string>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</json:string></affiliations></json:item><json:item><name>Timothy S. 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Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (VP16 activation domain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c-myc and c-fos genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.</abstract><qualityIndicators><score>9.328</score><pdfWordCount>4856</pdfWordCount><pdfCharCount>30962</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595 x 842 pts (A4)</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>206</abstractWordCount><abstractCharCount>1443</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Generation and characterization of a constitutively active Stat3 protein</title><genre><json:string>research-article</json:string></genre><host><title>Molecular Biology 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Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (VP16 activation domain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c-myc and c-fos genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><item><term>transcription factor</term></item><item><term>signal transduction</term></item><item><term>phosphoprotein</term></item><item><term>tyrosine kinase</term></item><item><term>oncogene</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Life Sciences</head><item><term>Animal Biochemistry</term></item><item><term>Animal Anatomy / Morphology / Histology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change 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AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Timothy</GivenName><GivenName>S.</GivenName><FamilyName>Schaefer</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Departments of Neurosurgery and Molecular Genetics</OrgDivision><OrgName>UT M.D. Anderson Cancer Center</OrgName><OrgAddress><Postbox>Box 11</Postbox><Street>1515 Holcombe Blvd.</Street><City>Houston</City><State>TX</State><Postcode>77030</Postcode><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Stats are latent transcription factors involved in normal cellular signaling in response to cytokine or growth factor stimulation. Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (<Emphasis Type="Italic">V</Emphasis>P16 <Emphasis Type="Italic">a</Emphasis>ctivation <Emphasis Type="Italic">d</Emphasis>omain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c<Emphasis Type="Italic">-myc</Emphasis> and c<Emphasis Type="Italic">-fos</Emphasis> genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.</Para></Abstract><KeywordGroup Language="En"><Keyword>transcription factor</Keyword><Keyword>signal transduction</Keyword><Keyword>phosphoprotein</Keyword><Keyword>tyrosine kinase</Keyword><Keyword>oncogene</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Generation and characterization of a constitutively active Stat3 protein</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Generation and characterization of a constitutively active Stat3 protein</title></titleInfo><name type="personal"><namePart type="given">Juan</namePart><namePart type="given">A.</namePart><namePart type="family">Barboza</namePart><affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shuguang</namePart><namePart type="family">Wang</namePart><affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Timothy</namePart><namePart type="given">S.</namePart><namePart type="family">Schaefer</namePart><affiliation>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" 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>Kluwer Academic Publishers</publisher><place><placeTerm type="text">Dordrecht</placeTerm></place><dateIssued encoding="w3cdtf">2004-03-01</dateIssued><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Stats are latent transcription factors involved in normal cellular signaling in response to cytokine or growth factor stimulation. Constitutive activation of Stats (primarily Stat3 and Stat5) has been implicated in growth dysregulation and oncogenesis. Furthermore, increased activation of Stats has been observed in several human tumors and tumor-derived cell lines. To assess the contribution of aberrant Stat activation in oncogenesis, we have created a chimeric molecule between Stat3β and a portion of the Herpes simplex virus VP16 activation domain. The resulting protein, Stat3β-VAD (VP16 activation domain), is tyrosine phosphorylated on Y705 and can bind DNA in the absence of upstream activation by c-Src or epidermal growth factor (EGF). Unlike Stat3α and Stat3β, Stat3β-VAD robustly activates transcription of several reporter genes without cytokine or growth factor stimulation. In addition, we show marked upregulation of the endogenous c-myc and c-fos genes upon inducible expression of Stat3β-VAD in COS-7 cells. Our protein displays the constitutive transcriptional activation of Stat3α seen in human tumors and will be a valuable tool in screens for Stat3-regulated genes. In response to the established Stat3 involvement in human cancers, Stat3β-VAD will also facilitate assessing the contribution of other cancer signaling cascades in the context of aberrant Stat3α activity in cancer development and progression.</abstract><subject lang="en"><topic>transcription factor</topic><topic>signal transduction</topic><topic>phosphoprotein</topic><topic>tyrosine kinase</topic><topic>oncogene</topic></subject><relatedItem type="host"><titleInfo><title>Molecular Biology Reports</title><subTitle>An International Journal on Molecular and Cellular Biology</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mol Biol Rep</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>Springer</publisher><dateIssued encoding="w3cdtf">2004-03-01</dateIssued><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><subject><genre>Life Sciences</genre><topic>Animal Biochemistry</topic><topic>Animal Anatomy / Morphology / Histology</topic></subject><identifier type="ISSN">0301-4851</identifier><identifier type="eISSN">1573-4978</identifier><identifier type="JournalID">11033</identifier><identifier type="IssueArticleCount">9</identifier><identifier type="VolumeIssueCount">2</identifier><part><date>2004</date><detail type="volume"><number>31</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>13</start><end>21</end></extent></part><recordInfo><recordOrigin>Kluwer Academic Publishers, 2004</recordOrigin></recordInfo></relatedItem><identifier type="istex">19514631FEA48FE7D9822F872ED4A4EACD22306C</identifier><identifier type="ark">ark:/67375/VQC-HPX0XKNG-9</identifier><identifier type="DOI">10.1023/B:MOLE.0000013503.16301.82</identifier><identifier type="ArticleID">5149851</identifier><identifier type="ArticleID">Art2</identifier><accessCondition type="use and reproduction" contentType="copyright">Kluwer Academic Publishers, 2004</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Kluwer Academic Publishers, 2004</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-HPX0XKNG-9/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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