| http://purl.uniprot.org/citations/15111299 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15111299 | http://www.w3.org/2000/01/rdf-schema#comment | "Mice lacking the vascular endothelial growth factor (VEGF) receptor flt-1 (VEGFR-1) die from vascular overgrowth, caused primarily by aberrant endothelial cell division (Kearney JB, Ambler CA, Monaco KA, Johnson N, Rapoport RG, Bautch VL: Vascular endothelial growth factor receptor Flt-1 negatively regulates developmental blood vessel formation by modulating endothelial cell division. Blood 2002, 99:2397-2407). Because a second high-affinity VEGF receptor, flk-1, produces a positive endothelial proliferation signal, it was logical to ask whether flt-1 affects developmental blood vessel formation by modulating signaling through flk-1. Differentiated embryonic stem cell cultures lacking flt-1 (flt-1-/-) had increased flk-1 tyrosine phosphorylation, indicating that flk-1 signaling is up-regulated in the mutant background. The selective flk-1 inhibitor SU5416 partially rescued the flt-1-/-mutant phenotype, and this rescue was accompanied by a decrease in the relative amount of flk-1 tyrosine phosphorylation. Thus reduced flk-1 signal transduction can partially compensate for the lack of flt-1. The flt-1-/-mutant phenotype was also partially rescued by Flt-1/Fc, a truncated flt-1 that binds and sequesters the VEGF ligand. Taken together, these data show that down-regulation of flk-1 signaling by two different strategies partially rescues the developmental vascular overgrowth seen in the absence of flt-1, and they support a model whereby flt-1 modulates the flk-1 signal at an early point in the pathway."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0002-9440(10)63711-x"xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Kumar R."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Roberts D.M."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Rosenberg M.P."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Bautch V.L."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Johnson J.H."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/author | "Kearney J.B."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/name | "Am J Pathol"xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/pages | "1531-1535"xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/title | "The vascular endothelial growth factor (VEGF) receptor Flt-1 (VEGFR-1) modulates Flk-1 (VEGFR-2) signaling during blood vessel formation."xsd:string |
| http://purl.uniprot.org/citations/15111299 | http://purl.uniprot.org/core/volume | "164"xsd:string |
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