File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cloning and expression of a rat Smad1: Regulation by TGFβ and modulation by the Ras/MEK pathway

TitleCloning and expression of a rat Smad1: Regulation by TGFβ and modulation by the Ras/MEK pathway
Authors
Issue Date1999
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 1999, v. 178 n. 3, p. 387-396 How to Cite?
AbstractA new family of signaling intermediates for TGFβ superfamily members and other growth factors has recently been identified and termed Smads. It has been suggested that the Smad1 subfamily is regulated primarily by the TGFβ superfamily member bone morphogenetic protein (BMP). Here we demonstrate that TGFβ induced phosphorylation of endogenous Smad1 in untransformed IECs and that the RI and RII TGFβ receptors were detectable in Smad1 immunocomplexes. Expression of a dominant-negative mutant of Ras inhibited the ability of TGFβ to phosphorylate endogenous Smad1. In a separate series of experiments, we have cloned a rat homologue of the drosophila mad gene (termed RSmad1) by screening an intestinal epithelial cell (IEC) cDNA library. By using an in vitro kinase assay with RSmad1 as the substrate, we demonstrate that the TGFβ receptor complex can directly phosphorylate RSmad1. We show, further, that a dominant-negative mutant of MEK1 inhibited the ability of RSmad1 to induce the TGFβ-responsive reporter p3TP-Lux in a human breast cancer cell line. Collectively, our data demonstrate that TGFβ can regulate Smad1 and that the Ras and MEK signaling components are partially required for the ability of TGFβ to regulate Smad1.
Persistent Identifierhttp://hdl.handle.net/10722/171667
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
References

 

DC FieldValueLanguage
dc.contributor.authorYue, Jen_US
dc.contributor.authorHartsouch, MTen_US
dc.contributor.authorFrey, RSen_US
dc.contributor.authorFrielle, Ten_US
dc.contributor.authorMulder, KMen_US
dc.date.accessioned2012-10-30T06:16:15Z-
dc.date.available2012-10-30T06:16:15Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Cellular Physiology, 1999, v. 178 n. 3, p. 387-396en_US
dc.identifier.issn0021-9541en_US
dc.identifier.urihttp://hdl.handle.net/10722/171667-
dc.description.abstractA new family of signaling intermediates for TGFβ superfamily members and other growth factors has recently been identified and termed Smads. It has been suggested that the Smad1 subfamily is regulated primarily by the TGFβ superfamily member bone morphogenetic protein (BMP). Here we demonstrate that TGFβ induced phosphorylation of endogenous Smad1 in untransformed IECs and that the RI and RII TGFβ receptors were detectable in Smad1 immunocomplexes. Expression of a dominant-negative mutant of Ras inhibited the ability of TGFβ to phosphorylate endogenous Smad1. In a separate series of experiments, we have cloned a rat homologue of the drosophila mad gene (termed RSmad1) by screening an intestinal epithelial cell (IEC) cDNA library. By using an in vitro kinase assay with RSmad1 as the substrate, we demonstrate that the TGFβ receptor complex can directly phosphorylate RSmad1. We show, further, that a dominant-negative mutant of MEK1 inhibited the ability of RSmad1 to induce the TGFβ-responsive reporter p3TP-Lux in a human breast cancer cell line. Collectively, our data demonstrate that TGFβ can regulate Smad1 and that the Ras and MEK signaling components are partially required for the ability of TGFβ to regulate Smad1.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_US
dc.relation.ispartofJournal of Cellular Physiologyen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCarrier Proteinsen_US
dc.subject.meshCell Cycle Proteinsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCloning, Molecularen_US
dc.subject.meshDna-Binding Proteins - Chemistry - Genetics - Metabolismen_US
dc.subject.meshDrosophilaen_US
dc.subject.meshGene Expression Regulation - Drug Effects - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMap Kinase Kinase 1en_US
dc.subject.meshMaleen_US
dc.subject.meshMitogen-Activated Protein Kinase Kinasesen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshNuclear Proteins - Chemistry - Geneticsen_US
dc.subject.meshOrgan Specificityen_US
dc.subject.meshPhosphoproteins - Chemistry - Geneticsen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Metabolismen_US
dc.subject.meshProtein-Tyrosine Kinases - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRecombinant Fusion Proteins - Biosynthesis - Chemistry - Metabolismen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshSequence Alignmenten_US
dc.subject.meshSequence Homology, Amino Aciden_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.subject.meshSmad Proteinsen_US
dc.subject.meshSmad1 Proteinen_US
dc.subject.meshTrans-Activators - Chemistry - Genetics - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTransforming Growth Factor Beta - Pharmacology - Physiologyen_US
dc.subject.meshRas Proteins - Metabolismen_US
dc.titleCloning and expression of a rat Smad1: Regulation by TGFβ and modulation by the Ras/MEK pathwayen_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.doi10.1002/(SICI)1097-4652(199903)178:3<387::AID-JCP13>3.0.CO;2-8en_US
dc.identifier.pmid9989785-
dc.identifier.scopuseid_2-s2.0-0032907437en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032907437&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume178en_US
dc.identifier.issue3en_US
dc.identifier.spage387en_US
dc.identifier.epage396en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYue, J=7101875828en_US
dc.identifier.scopusauthoridHartsouch, MT=6505473410en_US
dc.identifier.scopusauthoridFrey, RS=7201607576en_US
dc.identifier.scopusauthoridFrielle, T=6701554667en_US
dc.identifier.scopusauthoridMulder, KM=7005187184en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats