| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-102 |
Sentence |
denotes |
Identification of vascular endothelial growth factor determinants for binding KDR and FLT-1 receptors. |
| T2 |
103-179 |
Sentence |
denotes |
Generation of receptor-selective VEGF variants by site-directed mutagenesis. |
| T3 |
180-295 |
Sentence |
denotes |
Vascular endothelial growth factor (VEGF) expression in various cell types is induced by hypoxia and other stimuli. |
| T4 |
296-521 |
Sentence |
denotes |
VEGF mediates endothelial cell proliferation, angiogenesis, vascular growth, and vascular permeability via the endothelial cell receptors, kinase insert domain-containing receptor (KDR)/fetal liver kinase 1 (Flk-1) and FLT-1. |
| T5 |
522-644 |
Sentence |
denotes |
Alanine-scanning mutagenesis was used to identify a positively charged surface in VEGF that mediates binding to KDR/Flk-1. |
| T6 |
645-840 |
Sentence |
denotes |
Arg82, Lys84 and His86, located in a hairpin loop, were found to be critical for binding KDR/Flk-1, while negatively charged residues, Asp63, Glu64, and Glu67, were associated with FLT-1 binding. |
| T7 |
841-990 |
Sentence |
denotes |
A VEGF model based on PDGFb indicated these positively and negatively charged regions are distal in the monomer but are spatially close in the dimer. |
| T8 |
991-1124 |
Sentence |
denotes |
Mutations within the KDR site had minimal effect on FLT-1 binding, and mutants deficient in FLT-1 binding did not affect KDR binding. |
| T9 |
1125-1263 |
Sentence |
denotes |
Endothelial cell mitogenesis was abolished in mutants lacking KDR affinity; however, FLT-1 deficient mutants induced normal proliferation. |
| T10 |
1264-1422 |
Sentence |
denotes |
These results suggest dual sets of determinants in the VEGF dimer that cross-link cell surface receptors, triggering endothelial cell growth and angiogenesis. |
| T11 |
1423-1544 |
Sentence |
denotes |
Furthermore, this mutational analysis implicates KDR, but not FLT-1, in VEGF induction of endothelial cell proliferation. |
| T1 |
0-102 |
Sentence |
denotes |
Identification of vascular endothelial growth factor determinants for binding KDR and FLT-1 receptors. |
| T2 |
103-179 |
Sentence |
denotes |
Generation of receptor-selective VEGF variants by site-directed mutagenesis. |
| T3 |
180-295 |
Sentence |
denotes |
Vascular endothelial growth factor (VEGF) expression in various cell types is induced by hypoxia and other stimuli. |
| T4 |
296-521 |
Sentence |
denotes |
VEGF mediates endothelial cell proliferation, angiogenesis, vascular growth, and vascular permeability via the endothelial cell receptors, kinase insert domain-containing receptor (KDR)/fetal liver kinase 1 (Flk-1) and FLT-1. |
| T5 |
522-644 |
Sentence |
denotes |
Alanine-scanning mutagenesis was used to identify a positively charged surface in VEGF that mediates binding to KDR/Flk-1. |
| T6 |
645-840 |
Sentence |
denotes |
Arg82, Lys84 and His86, located in a hairpin loop, were found to be critical for binding KDR/Flk-1, while negatively charged residues, Asp63, Glu64, and Glu67, were associated with FLT-1 binding. |
| T7 |
841-990 |
Sentence |
denotes |
A VEGF model based on PDGFb indicated these positively and negatively charged regions are distal in the monomer but are spatially close in the dimer. |
| T8 |
991-1124 |
Sentence |
denotes |
Mutations within the KDR site had minimal effect on FLT-1 binding, and mutants deficient in FLT-1 binding did not affect KDR binding. |
| T9 |
1125-1263 |
Sentence |
denotes |
Endothelial cell mitogenesis was abolished in mutants lacking KDR affinity; however, FLT-1 deficient mutants induced normal proliferation. |
| T10 |
1264-1422 |
Sentence |
denotes |
These results suggest dual sets of determinants in the VEGF dimer that cross-link cell surface receptors, triggering endothelial cell growth and angiogenesis. |
| T11 |
1423-1544 |
Sentence |
denotes |
Furthermore, this mutational analysis implicates KDR, but not FLT-1, in VEGF induction of endothelial cell proliferation. |