| http://purl.uniprot.org/citations/11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11689702 | http://www.w3.org/2000/01/rdf-schema#comment | "The FOP-fibroblast growth factor receptor 1 (FGFR1) fusion protein is expressed as a consequence of a t(6;8) (q27;p12) translocation associated with a stem cell myeloproliferative disorder with lymphoma, myeloid hyperplasia and eosinophilia. In the present report, we show that the fusion of the leucine-rich N-terminal region of FOP to the catalytic domain of FGFR1 results in conversion of murine hematopoietic cell line Ba/F3 to factor-independent cell survival via an antiapoptotic effect. This survival effect is dependent upon the constitutive tyrosine phosphorylation of FOP-FGFR1. Phosphorylation of STAT1 and of STAT3, but not STAT5, is observed in cells expressing FOP-FGFR1. The survival function of FOP-FGFR1 is abrogated by mutation of the phospholipase C gamma binding site. Mitogen-activated protein kinase (MAPK) is also activated in FOP-FGFR1-expressing cells and confers cytokine-independent survival to hematopoietic cells. These results demonstrate that FOP-FGFR1 is capable of protecting cells from apoptosis by using the same effectors as the wild-type FGFR1. Furthermore, we show that FOP-FGFR1 phosphorylates phosphatidylinositol 3 (PI3)-kinase and AKT and that specific inhibitors of PI3-kinase impair its ability to promote cell survival. In addition, FOP-FGFR1-expressing cells show constitutive phosphorylation of the positive regulator of translation p70S6 kinase; this phosphorylation is inhibited by PI3-kinase and mTOR (mammalian target of rapamycin) inhibitors. These results indicate that translation control is important to mediate the cell survival effect induced by FOP-FGFR1. Finally, FOP-FGFR1 protects cells from apoptosis by survival signals including BCL2 overexpression and inactivation of caspase-9 activity. Elucidation of signaling events downstream of FOP-FGFR1 constitutive activation provides insight into the mechanism of leukemogenesis mediated by this oncogenic fusion protein."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.21.23.8129-8142.2001"xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/author | "Borg J.P."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/author | "Ollendorff V."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/author | "Birnbaum D."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/author | "Guasch G."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/author | "Pebusque M.J."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/name | "Mol Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/pages | "8129-8142"xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/title | "8p12 stem cell myeloproliferative disorder: the FOP-fibroblast growth factor receptor 1 fusion protein of the t(6;8) translocation induces cell survival mediated by mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt/mTOR pathways."xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://purl.uniprot.org/core/volume | "21"xsd:string |
| http://purl.uniprot.org/citations/11689702 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11689702 |
| http://purl.uniprot.org/citations/11689702 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11689702 |
| http://purl.uniprot.org/uniprot/#_O15164-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_P21781-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_P42224-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_P09038-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_Q7Z7A1-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_O95429-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_P27986-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_Q13480-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_O76093-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |
| http://purl.uniprot.org/uniprot/#_O95684-mappedCitation-11689702 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11689702 |