| http://purl.uniprot.org/citations/11751851 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11751851 | http://www.w3.org/2000/01/rdf-schema#comment | "We previously demonstrated in T47D cells transfected to express the transforming growth factor-beta receptor type II (TGF-betaRII) that insulin-like growth factor binding protein-3 (IGFBP-3) could stimulate Smad2 and Smad3 phosphorylation, potentiate TGF-beta1-stimulated Smad phosphorylation, and cooperate with exogenous TGF-beta1 in cell growth inhibition (Fanayan, S., Firth, S. M., Butt, A. J., and Baxter, R. C. (2000) J. Biol. Chem. 275, 39146-39151). This study further explores IGFBP-3 signaling through the Smad pathway. Like TGF-beta1, natural and recombinant IGFBP-3 stimulated the time- and dose-dependent phosphorylation of TGF-betaR1 as well as Smad2 and Smad3. This effect required the presence of TGF-betaRII. IGFBP-3 mutated in carboxyl-terminal nuclear localization signal residues retained activity in TGF-betaR1 and Smad phosphorylation, whereas IGFBP-5 was inactive. Immunoneutralization of endogenous TGF-beta1 suggested that TGF-beta1 was not essential for IGFBP-3 stimulation of this pathway, but it increased the effect of IGFBP-3. IGFBP-3, like TGF-beta1, elicited a rapid decline in immunodetectable Smad4 and Smad4.Smad2 complexes. IGFBP-3 and nuclear localization signal mutant IGFBP-3 stimulated the activation of the plasminogen activator inhibitor-1 promoter but was not additive with TGF-beta, suggesting that this end point is not a direct marker of the IGFBP-3 effect on cell proliferation. This study defines a signaling pathway for IGFBP-3 from a cell surface receptor to nuclear transcriptional activity, requiring TGF-betaRII but not dependent on the nuclear translocation of IGFBP-3. The precise mechanism by which IGFBP-3 interacts with the TGF-beta receptor system remains to be established."xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m108038200"xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/author | "Baxter R.C."xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/author | "Firth S.M."xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/author | "Fanayan S."xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/pages | "7255-7261"xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/title | "Signaling through the Smad pathway by insulin-like growth factor-binding protein-3 in breast cancer cells. Relationship to transforming growth factor-beta 1 signaling."xsd:string |
| http://purl.uniprot.org/citations/11751851 | http://purl.uniprot.org/core/volume | "277"xsd:string |
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