Title : Transactivation of the epidermal growth factor receptor in colonic epithelial cells by carbachol requires extracellular release of transforming growth factor-alpha.

Pub. Date : 2002 Nov 8

PMID : 12202486






14 Functional Relationships(s)
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1 Transactivation of the epidermal growth factor receptor in colonic epithelial cells by carbachol requires extracellular release of transforming growth factor-alpha. Carbachol epidermal growth factor receptor Homo sapiens
2 We have shown previously that the muscarinic agonist, carbachol (CCh), transactivates the epidermal growth factor receptor (EGFr) via calmodulin, Pyk-2, and Src kinase activation. Carbachol epidermal growth factor receptor Homo sapiens
3 We have shown previously that the muscarinic agonist, carbachol (CCh), transactivates the epidermal growth factor receptor (EGFr) via calmodulin, Pyk-2, and Src kinase activation. Carbachol epidermal growth factor receptor Homo sapiens
4 We have shown previously that the muscarinic agonist, carbachol (CCh), transactivates the epidermal growth factor receptor (EGFr) via calmodulin, Pyk-2, and Src kinase activation. Carbachol epidermal growth factor receptor Homo sapiens
5 We have shown previously that the muscarinic agonist, carbachol (CCh), transactivates the epidermal growth factor receptor (EGFr) via calmodulin, Pyk-2, and Src kinase activation. Carbachol epidermal growth factor receptor Homo sapiens
6 EGFr phosphorylation causes extracellular signal-regulated kinase (ERK) activation and inhibits CCh-stimulated chloride secretion across intestinal epithelial cells. Carbachol epidermal growth factor receptor Homo sapiens
7 Here we investigated whether CCh-stimulated EGFr transactivation involves EGFr ligand release. Carbachol epidermal growth factor receptor Homo sapiens
8 Here we investigated whether CCh-stimulated EGFr transactivation involves EGFr ligand release. Carbachol epidermal growth factor receptor Homo sapiens
9 Pre-incubation of T(84) cell monolayers with a neutralizing antibody to the EGFr ligand binding domain decreased CCh-induced phosphorylation of EGFr and ERK. Carbachol epidermal growth factor receptor Homo sapiens
10 Pre-incubation of T(84) cell monolayers with a neutralizing antibody to the EGFr ligand binding domain decreased CCh-induced phosphorylation of EGFr and ERK. Carbachol epidermal growth factor receptor Homo sapiens
11 CCh-stimulated efflux of (86)Rb+ from T(84) cell monolayers, which parallels changes in chloride secretion, was potentiated by anti-EGFr pre-incubation. Carbachol epidermal growth factor receptor Homo sapiens
12 Co-incubation with the Src kinase inhibitor PP2 and anti-EGFr had an additive inhibitory effect on CCh-induced ERK phosphorylation greater than either inhibitor alone. Carbachol epidermal growth factor receptor Homo sapiens
13 We conclude that CCh-stimulated EGFr transactivation and subsequent ERK activation, a pathway that limits CCh-induced chloride secretion, is mediated by metalloproteinase-dependent extracellular release of TGF-alpha and intracellular Src activation. Carbachol epidermal growth factor receptor Homo sapiens
14 We conclude that CCh-stimulated EGFr transactivation and subsequent ERK activation, a pathway that limits CCh-induced chloride secretion, is mediated by metalloproteinase-dependent extracellular release of TGF-alpha and intracellular Src activation. Carbachol epidermal growth factor receptor Homo sapiens