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Article: Cross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβ

TitleCross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβ
Authors
Issue Date1999
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 1999, v. 18 n. 11, p. 2033-2037 How to Cite?
AbstractOur previous data demonstrated that Ras activation was necessary and sufficient for transforming growth factor-β (TGFβ)-mediated Erk1 activation, and was required for TGFβ up-regulation of the Cdk inhibitors (CKI's) p27(kip1) and p21(Cip1). Here we examined the role of Ras in TGFβ-mediated effects on a rat homolog of Smad1 (termed RSmad1). We demonstrate that both TGFβ and bone morphogenetic protein (BMP) can induce endogenous Smad1 phosphorylation in intestinal epithelial cells (IECs). The combination of transient expression of RSmad1 and TGFβ treatment had an additive effect on induction of the TGFβ-responsive reporter 3TP-lux. Either inactivation of Ras by stable, inducible expression of a dominant-negative mutant of Ras (RasN17) or addition of MAP and ERK kinase (MEK) inhibitor PD98059 to cells significantly decreased the ability of both TGFβ and BMP to induce phosphorylation of endogenous Smad1 in IECs. Moreover, either inactivation of Res or addition of PD98059 to IEC 4-1 cells inhibited the ability of RSmad1 to regulate 3TP luciferase activity in both the presence and absence of TGFβ. Collectively, our data indicate that TGFβ can regulate RSmad1 function in epithelial cells, and that the Ras/MEK pathway is partially required for TGFβ-mediated regulation of RSmad1.
Persistent Identifierhttp://hdl.handle.net/10722/171671
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYue, Jen_US
dc.contributor.authorFrey, RSen_US
dc.contributor.authorMulder, KMen_US
dc.date.accessioned2012-10-30T06:16:16Z-
dc.date.available2012-10-30T06:16:16Z-
dc.date.issued1999en_US
dc.identifier.citationOncogene, 1999, v. 18 n. 11, p. 2033-2037en_US
dc.identifier.issn0950-9232en_US
dc.identifier.urihttp://hdl.handle.net/10722/171671-
dc.description.abstractOur previous data demonstrated that Ras activation was necessary and sufficient for transforming growth factor-β (TGFβ)-mediated Erk1 activation, and was required for TGFβ up-regulation of the Cdk inhibitors (CKI's) p27(kip1) and p21(Cip1). Here we examined the role of Ras in TGFβ-mediated effects on a rat homolog of Smad1 (termed RSmad1). We demonstrate that both TGFβ and bone morphogenetic protein (BMP) can induce endogenous Smad1 phosphorylation in intestinal epithelial cells (IECs). The combination of transient expression of RSmad1 and TGFβ treatment had an additive effect on induction of the TGFβ-responsive reporter 3TP-lux. Either inactivation of Ras by stable, inducible expression of a dominant-negative mutant of Ras (RasN17) or addition of MAP and ERK kinase (MEK) inhibitor PD98059 to cells significantly decreased the ability of both TGFβ and BMP to induce phosphorylation of endogenous Smad1 in IECs. Moreover, either inactivation of Res or addition of PD98059 to IEC 4-1 cells inhibited the ability of RSmad1 to regulate 3TP luciferase activity in both the presence and absence of TGFβ. Collectively, our data indicate that TGFβ can regulate RSmad1 function in epithelial cells, and that the Ras/MEK pathway is partially required for TGFβ-mediated regulation of RSmad1.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_US
dc.relation.ispartofOncogeneen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDna-Binding Proteins - Metabolismen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGenes, Reporteren_US
dc.subject.meshLuciferases - Geneticsen_US
dc.subject.meshMap Kinase Kinase 1en_US
dc.subject.meshMitogen-Activated Protein Kinase Kinasesen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshProtein-Tyrosine Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins P21(Ras) - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshSmad Proteinsen_US
dc.subject.meshSmad1 Proteinen_US
dc.subject.meshTrans-Activators - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta - Metabolismen_US
dc.titleCross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβen_US
dc.typeArticleen_US
dc.identifier.emailYue, J:jyue@hku.hken_US
dc.identifier.authorityYue, J=rp00286en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1202521-
dc.identifier.pmid10208426-
dc.identifier.scopuseid_2-s2.0-0033580393en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033580393&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issue11en_US
dc.identifier.spage2033en_US
dc.identifier.epage2037en_US
dc.identifier.isiWOS:000079191300014-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYue, J=7101875828en_US
dc.identifier.scopusauthoridFrey, RS=7201607576en_US
dc.identifier.scopusauthoridMulder, KM=7005187184en_US

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