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- Publisher Website: 10.1038/sj.onc.1202521
- Scopus: eid_2-s2.0-0033580393
- PMID: 10208426
- WOS: WOS:000079191300014
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Article: Cross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβ
Title | Cross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβ |
---|---|
Authors | |
Keywords | Ras/MEK Smad1 TGFβ |
Issue Date | 1999 |
Publisher | Nature 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? |
Abstract | Our 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 Identifier | http://hdl.handle.net/10722/171671 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 2.334 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yue, J | en_US |
dc.contributor.author | Frey, RS | en_US |
dc.contributor.author | Mulder, KM | en_US |
dc.date.accessioned | 2012-10-30T06:16:16Z | - |
dc.date.available | 2012-10-30T06:16:16Z | - |
dc.date.issued | 1999 | en_US |
dc.identifier.citation | Oncogene, 1999, v. 18 n. 11, p. 2033-2037 | en_US |
dc.identifier.issn | 0950-9232 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171671 | - |
dc.description.abstract | Our 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.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc | en_US |
dc.relation.ispartof | Oncogene | en_US |
dc.subject | Ras/MEK | - |
dc.subject | Smad1 | - |
dc.subject | TGFβ | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Dna-Binding Proteins - Metabolism | en_US |
dc.subject.mesh | Gene Expression Regulation | en_US |
dc.subject.mesh | Genes, Reporter | en_US |
dc.subject.mesh | Luciferases - Genetics | en_US |
dc.subject.mesh | Map Kinase Kinase 1 | en_US |
dc.subject.mesh | Mitogen-Activated Protein Kinase Kinases | en_US |
dc.subject.mesh | Protein-Serine-Threonine Kinases - Antagonists & Inhibitors - Metabolism | en_US |
dc.subject.mesh | Protein-Tyrosine Kinases - Antagonists & Inhibitors - Metabolism | en_US |
dc.subject.mesh | Proto-Oncogene Proteins P21(Ras) - Metabolism | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | Smad Proteins | en_US |
dc.subject.mesh | Smad1 Protein | en_US |
dc.subject.mesh | Trans-Activators - Metabolism | en_US |
dc.subject.mesh | Transforming Growth Factor Beta - Metabolism | en_US |
dc.title | Cross-talk between the Smad1 and Ras/MEK signaling pathways for TCFβ | en_US |
dc.type | Article | en_US |
dc.identifier.email | Yue, J:jyue@hku.hk | en_US |
dc.identifier.authority | Yue, J=rp00286 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1038/sj.onc.1202521 | - |
dc.identifier.pmid | 10208426 | - |
dc.identifier.scopus | eid_2-s2.0-0033580393 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0033580393&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 18 | en_US |
dc.identifier.issue | 11 | en_US |
dc.identifier.spage | 2033 | en_US |
dc.identifier.epage | 2037 | en_US |
dc.identifier.isi | WOS:000079191300014 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Yue, J=7101875828 | en_US |
dc.identifier.scopusauthorid | Frey, RS=7201607576 | en_US |
dc.identifier.scopusauthorid | Mulder, KM=7005187184 | en_US |
dc.identifier.issnl | 0950-9232 | - |