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PMID |
Sentence |
1 |
19341767
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The EGFR kinase inhibitor, AG1478, blocked activation of NHE-1, but did not block EGF-induced phosphorylation of Jak2 or CaM.
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2 |
19341767
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These results suggest that EGF induces NHE-1 activity in podocytes through two pathways: (1) EGF-->EGFR-->Jak2 activation (independent of EGFR tyrosine kinase activity)-->tyrosine phosphorylation of CaM-->CaM binding to NHE-1-->conformational change of NHE-1-->activation of NHE-1; and (2) EGF-->EGFR-->EGFR kinase activation-->association of CaM with NHE-1 (independent of Jak2)-->conformational change of NHE-1-->activation of NHE-1.
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3 |
20566668
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We show that BK2 receptor (BK2R) stimulation transactivates the epidermal growth factor receptor (EGFR).
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4 |
20566668
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EGFR transactivation is mediated by a disintegrin and metalloenzyme (ADAM) family members, which are required for both extracellular signal-regulated kinase (ERK) and EGFR activation by BK.
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5 |
20566668
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Using a gene-silencing approach we observed that both BK-induced ERK activation and BK-induced permeability decrease in podocytes is attenuated by ADAM17 down-regulation, and we identified epiregulin (ER) as the EGFR ligand participating in ADAM-dependent BK2R-EGFR cross-talk.
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6 |
20566668
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We propose that ZO-1 redistribution is an important element of BK-induced permeability change and the signaling events involved in ZO-1 rearrangement include transactivation of the EGFR via ADAM17 activation and ER shedding.
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7 |
19535569
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A disintegrin and metalloproteinase (ADAM)17 sheds growth factors from the cell membrane, including epidermal growth factor receptor (EGFR) ligand transforming growth factor (TGF)-alpha.
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8 |
19535569
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In mice, angiotensin II infusion induces renal fibrosis via ADAM17-mediated TGF-alpha shedding and subsequent EGFR activation.
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