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Matches in Nanopublications for { ?s ?p "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." ?g. }

• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.
• _5 value "Despite extensive overlap in the molecules recruited to the active receptors, there is some preferential modulation of signalling pathways. Tumour cells that express EGFR with kinase-domain mutations preferentially activate the pro-survival PI3K?AKT and signal transducer and activator of transcription (STAT) pathways67. Although EGFR has no consensus sequence for the p85 adaptor subunit of PI3K, it couples to this pathway through GAB1, which binds growth-factorreceptor- bound protein 2 (GRB2)." provenance.