| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-131 |
Sentence |
denotes |
NADPH-oxidase-dependent reactive oxygen species mediate EGFR transactivation by FPRL1 in WKYMVm-stimulated human lung cancer cells. |
| TextSentencer_T2 |
132-343 |
Sentence |
denotes |
Cross talk between unrelated cell surface receptors, such as G-protein-coupled receptors (GPCR) and receptor tyrosine kinases (RTK), is a crucial signaling mechanism to expand the cellular communication network. |
| TextSentencer_T3 |
344-504 |
Sentence |
denotes |
We investigated the ability of the GPCR formyl peptide receptor-like 1 (FPRL1) to transactivate the RTK epidermal growth factor receptor (EGFR) in CaLu-6 cells. |
| TextSentencer_T4 |
505-754 |
Sentence |
denotes |
We observed that stimulation with WKYMVm, an FPRL1 agonist isolated by screening synthetic peptide libraries, induces EGFR tyrosine phosphorylation, p47(phox) phosphorylation, NADPH-oxidase-dependent superoxide generation, and c-Src kinase activity. |
| TextSentencer_T5 |
755-891 |
Sentence |
denotes |
As a result of EGFR transactivation, phosphotyrosine residues provide docking sites for recruitment and triggering of the STAT3 pathway. |
| TextSentencer_T6 |
892-1040 |
Sentence |
denotes |
WKYMVm-induced EGFR transactivation is prevented by the FPRL1-selective antagonist WRWWWW, by pertussis toxin (PTX), and by the c-Src inhibitor PP2. |
| TextSentencer_T7 |
1041-1267 |
Sentence |
denotes |
The critical role of NADPH-oxidase-dependent superoxide generation in this cross-talk mechanism is corroborated by the finding that apocynin or a siRNA against p22(phox) prevents EGFR transactivation and c-Src kinase activity. |
| TextSentencer_T8 |
1268-1357 |
Sentence |
denotes |
In addition, WKYMVm promotes CaLu-6 cell growth, which is prevented by PTX and by WRWWWW. |
| TextSentencer_T9 |
1358-1572 |
Sentence |
denotes |
These results highlight the role of FPRL1 as a potential target of new drugs and suggest that targeting both FPRL1 and EGFR may yield superior therapeutic effects compared with targeting either receptor separately. |
| T1 |
0-131 |
Sentence |
denotes |
NADPH-oxidase-dependent reactive oxygen species mediate EGFR transactivation by FPRL1 in WKYMVm-stimulated human lung cancer cells. |
| T2 |
132-343 |
Sentence |
denotes |
Cross talk between unrelated cell surface receptors, such as G-protein-coupled receptors (GPCR) and receptor tyrosine kinases (RTK), is a crucial signaling mechanism to expand the cellular communication network. |
| T3 |
344-504 |
Sentence |
denotes |
We investigated the ability of the GPCR formyl peptide receptor-like 1 (FPRL1) to transactivate the RTK epidermal growth factor receptor (EGFR) in CaLu-6 cells. |
| T4 |
505-754 |
Sentence |
denotes |
We observed that stimulation with WKYMVm, an FPRL1 agonist isolated by screening synthetic peptide libraries, induces EGFR tyrosine phosphorylation, p47(phox) phosphorylation, NADPH-oxidase-dependent superoxide generation, and c-Src kinase activity. |
| T5 |
755-891 |
Sentence |
denotes |
As a result of EGFR transactivation, phosphotyrosine residues provide docking sites for recruitment and triggering of the STAT3 pathway. |
| T6 |
892-1040 |
Sentence |
denotes |
WKYMVm-induced EGFR transactivation is prevented by the FPRL1-selective antagonist WRWWWW, by pertussis toxin (PTX), and by the c-Src inhibitor PP2. |
| T7 |
1041-1267 |
Sentence |
denotes |
The critical role of NADPH-oxidase-dependent superoxide generation in this cross-talk mechanism is corroborated by the finding that apocynin or a siRNA against p22(phox) prevents EGFR transactivation and c-Src kinase activity. |
| T8 |
1268-1357 |
Sentence |
denotes |
In addition, WKYMVm promotes CaLu-6 cell growth, which is prevented by PTX and by WRWWWW. |
| T9 |
1358-1572 |
Sentence |
denotes |
These results highlight the role of FPRL1 as a potential target of new drugs and suggest that targeting both FPRL1 and EGFR may yield superior therapeutic effects compared with targeting either receptor separately. |