| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-126 |
Sentence |
denotes |
Phosphatidylinositol 3-kinase activity is required for hepatocyte growth factor-induced mitogenic signals in epithelial cells. |
| T2 |
127-248 |
Sentence |
denotes |
Phosphatidylinositol (PI) 3-kinase is an important enzyme implicated in growth factor-stimulated intracellular signaling. |
| T3 |
249-433 |
Sentence |
denotes |
In this study we have shown that hepatocyte growth factor (HGF) induces a rapid tyrosine phosphorylation of PI 3-kinase and association with HGF receptor/Met in Mv1Lu epithelial cells. |
| T4 |
434-563 |
Sentence |
denotes |
Murine mammary carcinoma (SP1) cells, which co-express HGF and HGF receptor/Met, showed sustained phosphorylation of PI 3-kinase. |
| T5 |
564-759 |
Sentence |
denotes |
Wortmannin, a potent inhibitor of PI 3-kinase, inhibited HGF-induced PI 3-kinase activity, proliferation of Mv1Lu cells, and spontaneous growth of SP1 cells in a dose-, and time-dependent manner. |
| T6 |
760-929 |
Sentence |
denotes |
Transfection of a dominant negative mutant p85 (Deltap85) subunit of PI 3-kinase into SP1 cells strongly inhibited HGF-stimulated proliferation and PI 3-kinase activity. |
| T7 |
930-997 |
Sentence |
denotes |
However, wortmannin did not influence HGF-induced c-Jun expression. |
| T8 |
998-1110 |
Sentence |
denotes |
Furthermore, HGF stimulated S6 kinase activity, but its activity was not required for HGF-induced proliferation. |
| T9 |
1111-1350 |
Sentence |
denotes |
Overall, these results suggest that HGF-induced PI 3-kinase activity is important for the mitogenic action of HGF in epithelial cells and further demonstrate that expression of c-Jun is not influenced by inhibition of PI 3-kinase activity. |
| T1 |
0-126 |
Sentence |
denotes |
Phosphatidylinositol 3-kinase activity is required for hepatocyte growth factor-induced mitogenic signals in epithelial cells. |
| T2 |
127-248 |
Sentence |
denotes |
Phosphatidylinositol (PI) 3-kinase is an important enzyme implicated in growth factor-stimulated intracellular signaling. |
| T3 |
249-433 |
Sentence |
denotes |
In this study we have shown that hepatocyte growth factor (HGF) induces a rapid tyrosine phosphorylation of PI 3-kinase and association with HGF receptor/Met in Mv1Lu epithelial cells. |
| T4 |
434-563 |
Sentence |
denotes |
Murine mammary carcinoma (SP1) cells, which co-express HGF and HGF receptor/Met, showed sustained phosphorylation of PI 3-kinase. |
| T5 |
564-759 |
Sentence |
denotes |
Wortmannin, a potent inhibitor of PI 3-kinase, inhibited HGF-induced PI 3-kinase activity, proliferation of Mv1Lu cells, and spontaneous growth of SP1 cells in a dose-, and time-dependent manner. |
| T6 |
760-929 |
Sentence |
denotes |
Transfection of a dominant negative mutant p85 (Deltap85) subunit of PI 3-kinase into SP1 cells strongly inhibited HGF-stimulated proliferation and PI 3-kinase activity. |
| T7 |
930-997 |
Sentence |
denotes |
However, wortmannin did not influence HGF-induced c-Jun expression. |
| T8 |
998-1110 |
Sentence |
denotes |
Furthermore, HGF stimulated S6 kinase activity, but its activity was not required for HGF-induced proliferation. |
| T9 |
1111-1350 |
Sentence |
denotes |
Overall, these results suggest that HGF-induced PI 3-kinase activity is important for the mitogenic action of HGF in epithelial cells and further demonstrate that expression of c-Jun is not influenced by inhibition of PI 3-kinase activity. |