Generation and characterization of a constitutively active Stat3 protein
Identifieur interne : 003157 ( Main/Exploration ); précédent : 003156; suivant : 003158Generation and characterization of a constitutively active Stat3 protein
Auteurs : Juan A. Barboza [États-Unis] ; Shuguang Wang [États-Unis] ; Timothy S. Schaefer [États-Unis]Source :
- 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
Affiliations:
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Barboza</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX</wicri:regionArea><wicri:noRegion>TX</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Shuguang" sort="Wang, Shuguang" uniqKey="Wang S" first="Shuguang" last="Wang">Shuguang Wang</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX</wicri:regionArea><wicri:noRegion>TX</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurosurgery and Molecular Genetics, UT M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 11, 77030, Houston, TX</wicri:regionArea><wicri:noRegion>TX</wicri:noRegion></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><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Barboza, Juan A" sort="Barboza, Juan A" uniqKey="Barboza J" first="Juan A." last="Barboza">Juan A. Barboza</name></noRegion><name sortKey="Schaefer, Timothy S" sort="Schaefer, Timothy S" uniqKey="Schaefer T" first="Timothy S." last="Schaefer">Timothy S. Schaefer</name><name sortKey="Wang, Shuguang" sort="Wang, Shuguang" uniqKey="Wang S" first="Shuguang" last="Wang">Shuguang Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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