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Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-85 Sentence denotes ERBB3-independent activation of the PI3K pathway in EGFR-mutant lung adenocarcinomas.
T1 0-85 Sentence denotes ERBB3-independent activation of the PI3K pathway in EGFR-mutant lung adenocarcinomas.
TextSentencer_T2 86-260 Sentence denotes ERBB3, a member of the EGFR family of receptor tyrosine kinases, has been implicated in activation of the PI3K pathway in human lung adenocarcinomas driven by EGFR mutations.
T2 86-260 Sentence denotes ERBB3, a member of the EGFR family of receptor tyrosine kinases, has been implicated in activation of the PI3K pathway in human lung adenocarcinomas driven by EGFR mutations.
TextSentencer_T3 261-465 Sentence denotes We investigated the contribution of ERBB3 to the initiation, progression, and therapeutic response of EGFR-induced lung adenocarcinomas using tetracycline- and tamoxifen-inducible transgenic mouse models.
T3 261-465 Sentence denotes We investigated the contribution of ERBB3 to the initiation, progression, and therapeutic response of EGFR-induced lung adenocarcinomas using tetracycline- and tamoxifen-inducible transgenic mouse models.
TextSentencer_T4 466-623 Sentence denotes Deletion of Erbb3 at the time of induction of mutant EGFR had no effect on tumorigenesis, demonstrating that ERBB3 is not required to initiate tumorigenesis.
T4 466-623 Sentence denotes Deletion of Erbb3 at the time of induction of mutant EGFR had no effect on tumorigenesis, demonstrating that ERBB3 is not required to initiate tumorigenesis.
TextSentencer_T5 624-772 Sentence denotes Tumors that developed in the absence of ERBB3 remained sensitive to EGFR tyrosine kinase inhibitors and retained activation of the PI3K-AKT pathway.
T5 624-772 Sentence denotes Tumors that developed in the absence of ERBB3 remained sensitive to EGFR tyrosine kinase inhibitors and retained activation of the PI3K-AKT pathway.
TextSentencer_T6 773-882 Sentence denotes Interestingly, acute loss of Erbb3 suppressed further growth of established EGFR(L858R)-mediated lung tumors.
T6 773-882 Sentence denotes Interestingly, acute loss of Erbb3 suppressed further growth of established EGFR(L858R)-mediated lung tumors.
TextSentencer_T7 883-1141 Sentence denotes Four weeks after deletion of Erbb3, the tumors exhibited phosphorylation of EGFR, of the adaptor proteins GAB1 and GAB2, and of the downstream signaling molecules AKT and ERK, suggesting that alternative signaling pathways could compensate for loss of Erbb3.
T7 883-1141 Sentence denotes Four weeks after deletion of Erbb3, the tumors exhibited phosphorylation of EGFR, of the adaptor proteins GAB1 and GAB2, and of the downstream signaling molecules AKT and ERK, suggesting that alternative signaling pathways could compensate for loss of Erbb3.
TextSentencer_T8 1142-1335 Sentence denotes Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines.
T8 1142-1335 Sentence denotes Similar to our observations with mouse tumors, we found that GAB adaptor proteins play a role in ERBB3-independent activation of the PI3K pathway by mutant EGFR in EGFR-mutant human cell lines.
TextSentencer_T9 1336-1606 Sentence denotes Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications.
T9 1336-1606 Sentence denotes Finally, in such cell lines, increased levels of phosphorylation of ERBB2 or MET were associated with reduced sensitivity to acute loss of ERBB3, suggesting remarkable plasticity in the signaling pathways regulated by mutant EGFR with important therapeutic implications.