| http://purl.uniprot.org/citations/16682955 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16682955 | http://www.w3.org/2000/01/rdf-schema#comment | "Fibroblast growth factor (FGF) signaling can bypass the requirement for estrogen receptor (ER) activation in the growth of ER-positive (ER+) breast cancer cells. Fibroblast growth factor-1 stimulation leads to phosphorylation of the adaptor protein Suc1-associated neurotrophic factor-induced tyrosine-phosphorylated target (SNT-1) on C-terminal tyrosine residues, whereas it is constitutively bound through its N-terminal phosphotyrosine-binding domain (PTB) to FGF receptors (FGFRs). By expressing the PTB domain of SNT-1 (SNT-1 PTB) in an inducible manner in an ER+ breast carcinoma line, ML20, we asked whether we could uncouple FGFR activation from its downstream signaling components and abrogate FGF-1-induced antiestrogen-resistant growth. Induction of SNT-1 PTB resulted in a significant decrease of FGF-1-dependent tyrosine phosphorylation of endogenous SNT-1, strong inhibition of complex formation between SNT-1, Gab-1 and Sos-1, and reduced activation of Ras, mitogen-activated protein kinase (MAP kinase), and Akt. SNT-1 PTB also inhibited the phosphorylation of p70S6K on Thr421/Ser424 and Ser411, which may result from the abrogation of MAP kinase activity. Moreover, we also observed a decreased phosphorylation of the MAP kinase-independent site Thr389. This may reflect both inhibition of PI-3 kinase pathways and mammalian target of rapamycin (mTOR)-dependent signaling, as the phosphorylation of Thr389 site was sensitive to treatment with the PI3-K and mTOR inhibitors, LY294002 and rapamycin, respectively. Collectively these results suggest that SNT-1 plays a pivotal role in FGF-dependent activation of the Ras-MAP kinase, PI-3 kinase, and mTOR pathways in these cells. Fibroblast growth factor-1 dependent colony formation of ML20 cells in media containing the pure antiestrogen ICI 182,780 was also markedly inhibited upon induction of SNT-1 PTB, suggesting that blockade of FGFR-SNT-1 interactions might abrogate FGF-mediated antiestrogen resistance in breast cancers."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.org/dc/terms/identifier | "doi:10.1038/sj.onc.1209592"xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Qu Z."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Hays S."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Kern F.G."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Manuvakhova M."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Thottassery J.V."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Westbrook L."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/author | "Rentz S.S."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/pages | "6003-6014"xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/title | "Expression of the SNT-1/FRS2 phosphotyrosine binding domain inhibits activation of MAP kinase and PI3-kinase pathways and antiestrogen resistant growth induced by FGF-1 in human breast carcinoma cells."xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://purl.uniprot.org/core/volume | "25"xsd:string |
| http://purl.uniprot.org/citations/16682955 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16682955 |
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