PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22511543-5 2012 Carbachol (CCh), a muscarinic receptor-specific agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathways involving caspase 3/7, but its cytoprotective effect was decreased by a M3R antagonist, a mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) inhibitor, a phosphatidylinositol 3-kinase/Akt inhibitor, or an epidermal growth factor receptor (EGFR) inhibitor. Carbachol 0-9 epidermal growth factor receptor Homo sapiens 385-417 22865467-3 2012 The inhibition of the epidermal growth factor receptor (EGFR) by AG1478 or protein kinase C (PKC) by GF109203X significantly reduced carbachol-stimulated ERK1/2 activation and cell proliferation. Carbachol 133-142 epidermal growth factor receptor Homo sapiens 22-54 22865467-3 2012 The inhibition of the epidermal growth factor receptor (EGFR) by AG1478 or protein kinase C (PKC) by GF109203X significantly reduced carbachol-stimulated ERK1/2 activation and cell proliferation. Carbachol 133-142 epidermal growth factor receptor Homo sapiens 56-60 22865467-4 2012 Cotreatment of the cells with AG1478 and GF109203X produced an additive effect on carbachol-stimulated ERK1/2 activation, suggesting that the EGFR and PKC pathways act in parallel. Carbachol 82-91 epidermal growth factor receptor Homo sapiens 142-146 22865467-6 2012 In SNU-407 cells, carbachol treatment induced RSK activation in an atropine-sensitive manner, and this RSK activation was decreased by the inhibition of either EGFR or PKC. Carbachol 18-27 epidermal growth factor receptor Homo sapiens 160-164 22511543-5 2012 Carbachol (CCh), a muscarinic receptor-specific agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathways involving caspase 3/7, but its cytoprotective effect was decreased by a M3R antagonist, a mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) inhibitor, a phosphatidylinositol 3-kinase/Akt inhibitor, or an epidermal growth factor receptor (EGFR) inhibitor. Carbachol 0-9 epidermal growth factor receptor Homo sapiens 419-423 22511543-5 2012 Carbachol (CCh), a muscarinic receptor-specific agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathways involving caspase 3/7, but its cytoprotective effect was decreased by a M3R antagonist, a mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) inhibitor, a phosphatidylinositol 3-kinase/Akt inhibitor, or an epidermal growth factor receptor (EGFR) inhibitor. Carbachol 11-14 epidermal growth factor receptor Homo sapiens 385-417 22511543-5 2012 Carbachol (CCh), a muscarinic receptor-specific agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathways involving caspase 3/7, but its cytoprotective effect was decreased by a M3R antagonist, a mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) inhibitor, a phosphatidylinositol 3-kinase/Akt inhibitor, or an epidermal growth factor receptor (EGFR) inhibitor. Carbachol 11-14 epidermal growth factor receptor Homo sapiens 419-423 22511543-6 2012 Ligation of M3R with CCh transactivated EGFR and phosphorylated ERK and Akt, the downstream targets of EGFR. Carbachol 21-24 epidermal growth factor receptor Homo sapiens 40-44 22511543-6 2012 Ligation of M3R with CCh transactivated EGFR and phosphorylated ERK and Akt, the downstream targets of EGFR. Carbachol 21-24 epidermal growth factor receptor Homo sapiens 103-107 22511543-8 2012 CCh stimulated Src phosphorylation and binding to EGFR. Carbachol 0-3 epidermal growth factor receptor Homo sapiens 50-54 19875701-7 2010 CCh-induced JNK phosphorylation was attenuated by the EGFR inhibitor, tyrphostin-AG1478 (1 microM). Carbachol 0-3 epidermal growth factor receptor Homo sapiens 54-58 20525722-6 2011 AG1478, a selective inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, inhibited carbachol-induced MUC5AC responses, indicating EGFR transactivation. Carbachol 100-109 epidermal growth factor receptor Homo sapiens 33-65 20525722-6 2011 AG1478, a selective inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, inhibited carbachol-induced MUC5AC responses, indicating EGFR transactivation. Carbachol 100-109 epidermal growth factor receptor Homo sapiens 67-71 20525722-6 2011 AG1478, a selective inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, inhibited carbachol-induced MUC5AC responses, indicating EGFR transactivation. Carbachol 100-109 epidermal growth factor receptor Homo sapiens 147-151 20525722-7 2011 Aclidinium inhibited carbachol-induced phospho-EGFR and phospho-p44/42 MAPK expression. Carbachol 21-30 epidermal growth factor receptor Homo sapiens 47-51 20939850-8 2011 Conditioned medium from CCh-pretreated cells mimicked its chronic antisecretory actions, suggesting involvement of an epithelial-derived soluble factor but further experimentation ruled out the involvement of epidermal growth factor receptor ligands. Carbachol 24-27 epidermal growth factor receptor Homo sapiens 209-241 19615971-2 2009 Treatment of T84 cells with the selective inhibitor of EGF receptor (EGFR) tyrosine kinase AG1478 abrogated Akt phosphorylation on Ser(473) induced by either carbachol or EGF, indicating that carbachol-induced Akt activation is mediated through EGFR transactivation. Carbachol 158-167 epidermal growth factor receptor Homo sapiens 55-67 19615971-2 2009 Treatment of T84 cells with the selective inhibitor of EGF receptor (EGFR) tyrosine kinase AG1478 abrogated Akt phosphorylation on Ser(473) induced by either carbachol or EGF, indicating that carbachol-induced Akt activation is mediated through EGFR transactivation. Carbachol 158-167 epidermal growth factor receptor Homo sapiens 69-73 19615971-2 2009 Treatment of T84 cells with the selective inhibitor of EGF receptor (EGFR) tyrosine kinase AG1478 abrogated Akt phosphorylation on Ser(473) induced by either carbachol or EGF, indicating that carbachol-induced Akt activation is mediated through EGFR transactivation. Carbachol 192-201 epidermal growth factor receptor Homo sapiens 55-67 19615971-2 2009 Treatment of T84 cells with the selective inhibitor of EGF receptor (EGFR) tyrosine kinase AG1478 abrogated Akt phosphorylation on Ser(473) induced by either carbachol or EGF, indicating that carbachol-induced Akt activation is mediated through EGFR transactivation. Carbachol 192-201 epidermal growth factor receptor Homo sapiens 69-73 17643958-5 2007 In addition, Cch-induced MAPK/ERK phosphorylation was partially inhibited by LY294002 and wortmannin, two selective inhibitors of phosphatidylinositol 3-kinase (PI3K), tyrphostin AG1478, a specific inhibitor of epidermal growth factor receptor (EGFR) kinase, and (-)-perillic acid, a post-translational inhibitor of small G-proteins isoprenylation. Carbachol 13-16 epidermal growth factor receptor Homo sapiens 211-243 17643958-5 2007 In addition, Cch-induced MAPK/ERK phosphorylation was partially inhibited by LY294002 and wortmannin, two selective inhibitors of phosphatidylinositol 3-kinase (PI3K), tyrphostin AG1478, a specific inhibitor of epidermal growth factor receptor (EGFR) kinase, and (-)-perillic acid, a post-translational inhibitor of small G-proteins isoprenylation. Carbachol 13-16 epidermal growth factor receptor Homo sapiens 245-249 12748850-9 2003 RESULTS: Carbachol induced tyrosine phosphorylation of EGFR, which was abolished by an EGFR tyrosine kinase inhibitor AG1478. Carbachol 9-18 epidermal growth factor receptor Homo sapiens 55-59 15389641-8 2005 CCh also induced association of FAK with the EGFr and FAK phosphorylation was attenuated by an EGFr inhibitor, tyrphostin AG1478, and an inhibitor of Src family kinases, PP2. Carbachol 0-3 epidermal growth factor receptor Homo sapiens 45-49 15389641-8 2005 CCh also induced association of FAK with the EGFr and FAK phosphorylation was attenuated by an EGFr inhibitor, tyrphostin AG1478, and an inhibitor of Src family kinases, PP2. Carbachol 0-3 epidermal growth factor receptor Homo sapiens 95-99 17307332-4 2007 Similarly, PKC inhibition enhanced EGFR transactivation in human colonic epithelial T84 cells stimulated with carbachol, as well as in bombesin-stimulated Rat-1 fibroblasts stably transfected with the bombesin receptor. Carbachol 110-119 epidermal growth factor receptor Homo sapiens 35-39 15389641-1 2005 We have previously shown that the Gq protein coupled receptor (GqPCR) agonist, carbachol (CCh), transactivates and recruits epidermal growth factor receptor (EGFr)-dependent signaling mechanisms in intestinal epithelial cells. Carbachol 79-88 epidermal growth factor receptor Homo sapiens 124-156 15389641-1 2005 We have previously shown that the Gq protein coupled receptor (GqPCR) agonist, carbachol (CCh), transactivates and recruits epidermal growth factor receptor (EGFr)-dependent signaling mechanisms in intestinal epithelial cells. Carbachol 79-88 epidermal growth factor receptor Homo sapiens 158-162 15389641-1 2005 We have previously shown that the Gq protein coupled receptor (GqPCR) agonist, carbachol (CCh), transactivates and recruits epidermal growth factor receptor (EGFr)-dependent signaling mechanisms in intestinal epithelial cells. Carbachol 90-93 epidermal growth factor receptor Homo sapiens 124-156 15389641-1 2005 We have previously shown that the Gq protein coupled receptor (GqPCR) agonist, carbachol (CCh), transactivates and recruits epidermal growth factor receptor (EGFr)-dependent signaling mechanisms in intestinal epithelial cells. Carbachol 90-93 epidermal growth factor receptor Homo sapiens 158-162 14517795-14 2003 CONCLUSIONS: GH inhibits CCh-induced chloride secretion via a JAK2-dependent mechanism involving transactivation of EGFr and consequent recruitment of ERK1/2. Carbachol 25-28 epidermal growth factor receptor Homo sapiens 116-120 12748850-9 2003 RESULTS: Carbachol induced tyrosine phosphorylation of EGFR, which was abolished by an EGFR tyrosine kinase inhibitor AG1478. Carbachol 9-18 epidermal growth factor receptor Homo sapiens 87-91 12748850-10 2003 Transactivation by carbachol was also abrogated by a metalloproteinases (MMPs) inhibitor GM6001 or an EGFR-blocking antibody (LA-1), suggesting that binding of EGFR ligand(s) produced by MMPs may initiate transactivation in a manner dependent on EGFR tyrosine kinase. Carbachol 19-28 epidermal growth factor receptor Homo sapiens 102-106 12748850-10 2003 Transactivation by carbachol was also abrogated by a metalloproteinases (MMPs) inhibitor GM6001 or an EGFR-blocking antibody (LA-1), suggesting that binding of EGFR ligand(s) produced by MMPs may initiate transactivation in a manner dependent on EGFR tyrosine kinase. Carbachol 19-28 epidermal growth factor receptor Homo sapiens 160-164 12748850-10 2003 Transactivation by carbachol was also abrogated by a metalloproteinases (MMPs) inhibitor GM6001 or an EGFR-blocking antibody (LA-1), suggesting that binding of EGFR ligand(s) produced by MMPs may initiate transactivation in a manner dependent on EGFR tyrosine kinase. Carbachol 19-28 epidermal growth factor receptor Homo sapiens 160-164 12202486-10 2002 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 17-20 epidermal growth factor receptor Homo sapiens 32-36 12388102-5 2003 CCh-induced p38 phosphorylation was attenuated by the EGFR inhibitor tyrphostin AG-1478 (0.1 nM-10 microM) and by the Src family kinase inhibitor PP2 (20 nM-2 microM). Carbachol 0-3 epidermal growth factor receptor Homo sapiens 54-58 12202486-0 2002 Transactivation of the epidermal growth factor receptor in colonic epithelial cells by carbachol requires extracellular release of transforming growth factor-alpha. Carbachol 87-96 epidermal growth factor receptor Homo sapiens 23-55 12202486-1 2002 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 54-63 epidermal growth factor receptor Homo sapiens 90-122 12202486-1 2002 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 54-63 epidermal growth factor receptor Homo sapiens 124-128 12202486-10 2002 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 106-109 epidermal growth factor receptor Homo sapiens 32-36 12202486-1 2002 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 65-68 epidermal growth factor receptor Homo sapiens 90-122 12202486-1 2002 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 65-68 epidermal growth factor receptor Homo sapiens 124-128 12202486-2 2002 EGFr phosphorylation causes extracellular signal-regulated kinase (ERK) activation and inhibits CCh-stimulated chloride secretion across intestinal epithelial cells. Carbachol 96-99 epidermal growth factor receptor Homo sapiens 0-4 12202486-3 2002 Here we investigated whether CCh-stimulated EGFr transactivation involves EGFr ligand release. Carbachol 29-32 epidermal growth factor receptor Homo sapiens 44-48 10816433-1 2000 The acetylcholine analogue carbachol rapidly activated mitogen-activated protein kinase (MAPK), and caused tyrosine phosphorylation of the adapter protein p52 Shc and the epidermalgrowth factor (EGF) receptor, in human embryonic kidney cells stably expressing m3 muscarinic receptors. Carbachol 27-36 epidermal growth factor receptor Homo sapiens 171-208 12202486-3 2002 Here we investigated whether CCh-stimulated EGFr transactivation involves EGFr ligand release. Carbachol 29-32 epidermal growth factor receptor Homo sapiens 74-78 12202486-4 2002 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 113-116 epidermal growth factor receptor Homo sapiens 76-80 12202486-4 2002 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 113-116 epidermal growth factor receptor Homo sapiens 144-148 12202486-5 2002 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 0-3 epidermal growth factor receptor Homo sapiens 132-136 12202486-7 2002 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 99-102 epidermal growth factor receptor Homo sapiens 57-61 10816433-5 2000 In co-stimulation experiments, carbachol and EGF activated MAPK in a non-additive fashion; moreover, EGF-induced association of Shc with the phosphorylated EGF receptor was inhibited by carbachol. Carbachol 186-195 epidermal growth factor receptor Homo sapiens 156-168 10816433-4 2000 In a subset of these experiments, GF109203X concomitantly increased carbachol-induced tyrosine phosphorylation of p52 Shc and the EGF receptor. Carbachol 68-77 epidermal growth factor receptor Homo sapiens 130-142 10816433-5 2000 In co-stimulation experiments, carbachol and EGF activated MAPK in a non-additive fashion; moreover, EGF-induced association of Shc with the phosphorylated EGF receptor was inhibited by carbachol. Carbachol 31-40 epidermal growth factor receptor Homo sapiens 156-168 10777553-9 2000 The Src family kinase inhibitor, PP2 (20 nM-20 microM) attenuated CCh-stimulated EGFR and ERK phosphorylation and potentiated chloride secretory responses to CCh. Carbachol 66-69 epidermal growth factor receptor Homo sapiens 81-85 10777553-0 2000 Carbachol-stimulated transactivation of epidermal growth factor receptor and mitogen-activated protein kinase in T(84) cells is mediated by intracellular Ca2+, PYK-2, and p60(src). Carbachol 0-9 epidermal growth factor receptor Homo sapiens 40-72 10777553-1 2000 Ca(2+)-dependent agonists, such as carbachol (CCh), stimulate epidermal growth factor receptor (EGFR) transactivation and mitogen-activated protein kinase activation in T(84) intestinal epithelial cells. Carbachol 35-44 epidermal growth factor receptor Homo sapiens 62-94 10777553-10 2000 We conclude that CCh-stimulated transactivation of the EGFR is mediated by a pathway involving elevations in intracellular Ca(2+), calmodulin, PYK-2, and p60(src). Carbachol 17-20 epidermal growth factor receptor Homo sapiens 55-59 10777553-1 2000 Ca(2+)-dependent agonists, such as carbachol (CCh), stimulate epidermal growth factor receptor (EGFR) transactivation and mitogen-activated protein kinase activation in T(84) intestinal epithelial cells. Carbachol 35-44 epidermal growth factor receptor Homo sapiens 96-100 10777553-1 2000 Ca(2+)-dependent agonists, such as carbachol (CCh), stimulate epidermal growth factor receptor (EGFR) transactivation and mitogen-activated protein kinase activation in T(84) intestinal epithelial cells. Carbachol 46-49 epidermal growth factor receptor Homo sapiens 62-94 9765228-9 1998 Immunoprecipitation/Western blot studies revealed that CCh stimulated tyrosine phosphorylation of the EGF receptor (EGFr) and increased co-immunoprecipitation of the adapter proteins, Shc and Grb2, with the EGFr. Carbachol 55-58 epidermal growth factor receptor Homo sapiens 102-114 10777553-1 2000 Ca(2+)-dependent agonists, such as carbachol (CCh), stimulate epidermal growth factor receptor (EGFR) transactivation and mitogen-activated protein kinase activation in T(84) intestinal epithelial cells. Carbachol 46-49 epidermal growth factor receptor Homo sapiens 96-100 10777553-3 2000 Here, we investigated mechanisms underlying CCh-stimulated epidermal growth factor receptor (EGFR) transactivation. Carbachol 44-47 epidermal growth factor receptor Homo sapiens 59-91 10777553-3 2000 Here, we investigated mechanisms underlying CCh-stimulated epidermal growth factor receptor (EGFR) transactivation. Carbachol 44-47 epidermal growth factor receptor Homo sapiens 93-97 10777553-6 2000 CCh (100 microM) stimulated tyrosine phosphorylation and association of the Ca(2+)-dependent tyrosine kinase, PYK-2, with the EGFR, which was inhibited by the Ca(2+) chelator, BAPTA (20 microM). Carbachol 0-3 epidermal growth factor receptor Homo sapiens 126-130 10777553-7 2000 The calmodulin inhibitor, fluphenazine (50 microM) inhibited CCh-stimulated PYK-2 association with the EGFR and phosphorylation of EGFR and ERK. Carbachol 61-64 epidermal growth factor receptor Homo sapiens 103-107 10777553-7 2000 The calmodulin inhibitor, fluphenazine (50 microM) inhibited CCh-stimulated PYK-2 association with the EGFR and phosphorylation of EGFR and ERK. Carbachol 61-64 epidermal growth factor receptor Homo sapiens 131-135 10777553-8 2000 CCh also induced tyrosine phosphorylation of p60(src) and association of p60(src) with both PYK-2 and the EGFR. Carbachol 0-3 epidermal growth factor receptor Homo sapiens 106-110 10622253-2 1999 The transactivation of epidermal growth factor receptor (EGFR)-dependent signalling pathways upon stimulation of G-protein-coupled receptors (GPCRs), which are critical for the mitogenic activity of ligands such as lysophosphatidic acid, endothelin, thrombin, bombesin and carbachol, provides evidence for such an interconnected communication network. Carbachol 273-282 epidermal growth factor receptor Homo sapiens 23-55 10622253-2 1999 The transactivation of epidermal growth factor receptor (EGFR)-dependent signalling pathways upon stimulation of G-protein-coupled receptors (GPCRs), which are critical for the mitogenic activity of ligands such as lysophosphatidic acid, endothelin, thrombin, bombesin and carbachol, provides evidence for such an interconnected communication network. Carbachol 273-282 epidermal growth factor receptor Homo sapiens 57-61 10049786-3 1999 Activation of muscarinic receptors with carbachol was found to inhibit EGF-induced signaling, including tyrosine phosphorylation of the adaptor protein Cbl and of the EGF receptor, and complex formation between Shc proteins and the EGF receptor and Grb2. Carbachol 40-49 epidermal growth factor receptor Homo sapiens 167-179 10049786-3 1999 Activation of muscarinic receptors with carbachol was found to inhibit EGF-induced signaling, including tyrosine phosphorylation of the adaptor protein Cbl and of the EGF receptor, and complex formation between Shc proteins and the EGF receptor and Grb2. Carbachol 40-49 epidermal growth factor receptor Homo sapiens 232-244 10559227-2 1999 The muscarinic agonist of chloride secretion, carbachol (CCh), also stimulates an antisecretory pathway that involves transactivation of the EGF receptor (EGFR) but does not involve PI3-K. Carbachol 46-55 epidermal growth factor receptor Homo sapiens 141-153 10559227-2 1999 The muscarinic agonist of chloride secretion, carbachol (CCh), also stimulates an antisecretory pathway that involves transactivation of the EGF receptor (EGFR) but does not involve PI3-K. Carbachol 46-55 epidermal growth factor receptor Homo sapiens 155-159 10559227-2 1999 The muscarinic agonist of chloride secretion, carbachol (CCh), also stimulates an antisecretory pathway that involves transactivation of the EGF receptor (EGFR) but does not involve PI3-K. Carbachol 57-60 epidermal growth factor receptor Homo sapiens 141-153 10559227-2 1999 The muscarinic agonist of chloride secretion, carbachol (CCh), also stimulates an antisecretory pathway that involves transactivation of the EGF receptor (EGFR) but does not involve PI3-K. Carbachol 57-60 epidermal growth factor receptor Homo sapiens 155-159 10559227-3 1999 Here, we have examined if ErbB receptors, other than the EGFR, have a role in regulation of colonic secretion and if differential effects on ErbB receptor activation may explain the ability of the EGFR to propagate diverse signaling pathways in response to EGF versus CCh. Carbachol 268-271 epidermal growth factor receptor Homo sapiens 197-201 10559227-7 1999 Further studies revealed that, while both EGF (100 ng/ml) and CCh (100 microM) stimulated phosphorylation of the EGFR, only EGF stimulated phosphorylation of ErbB2, and neither stimulated ErbB3 phosphorylation. Carbachol 62-65 epidermal growth factor receptor Homo sapiens 113-117 10559227-10 1999 Differential dimerization with other ErbB family members may underlie the ability of the EGFR to propagate diverse inhibitory signals in response to activation by EGF or transactivation by CCh. Carbachol 189-192 epidermal growth factor receptor Homo sapiens 37-41 10559227-10 1999 Differential dimerization with other ErbB family members may underlie the ability of the EGFR to propagate diverse inhibitory signals in response to activation by EGF or transactivation by CCh. Carbachol 189-192 epidermal growth factor receptor Homo sapiens 89-93 9765228-0 1998 Carbachol stimulates transactivation of epidermal growth factor receptor and mitogen-activated protein kinase in T84 cells. Carbachol 0-9 epidermal growth factor receptor Homo sapiens 40-72 9765228-9 1998 Immunoprecipitation/Western blot studies revealed that CCh stimulated tyrosine phosphorylation of the EGF receptor (EGFr) and increased co-immunoprecipitation of the adapter proteins, Shc and Grb2, with the EGFr. Carbachol 55-58 epidermal growth factor receptor Homo sapiens 116-120 9765228-9 1998 Immunoprecipitation/Western blot studies revealed that CCh stimulated tyrosine phosphorylation of the EGF receptor (EGFr) and increased co-immunoprecipitation of the adapter proteins, Shc and Grb2, with the EGFr. Carbachol 55-58 epidermal growth factor receptor Homo sapiens 207-211 9765228-10 1998 An inhibitor of EGFr phosphorylation, tyrphostin AG1478 (1 microM), reversed CCh-stimulated phosphorylation of both EGFr and ERK. Carbachol 77-80 epidermal growth factor receptor Homo sapiens 16-20 9765228-10 1998 An inhibitor of EGFr phosphorylation, tyrphostin AG1478 (1 microM), reversed CCh-stimulated phosphorylation of both EGFr and ERK. Carbachol 77-80 epidermal growth factor receptor Homo sapiens 116-120 9765228-12 1998 We conclude that CCh activates ERK in T84 cells via a mechanism involving transactivation of the EGFr, and that this pathway constitutes an inhibitory signaling pathway by which chloride secretory responses to CCh may be negatively regulated. Carbachol 17-20 epidermal growth factor receptor Homo sapiens 97-101 32911509-5 2020 The addition of carbachol or arecaidine propargyl ester, a non-selective or a selective subtype 2 muscarinic receptor agonist respectively, plus paclitaxel reduces cell viability involving a down-regulation in the expression of ATP "binding cassette" G2 drug transporter and epidermal growth factor receptor. Carbachol 16-25 epidermal growth factor receptor Homo sapiens 275-307 32652816-3 2020 EGFr TKIs (such as afatinib, erlotinib, and osimertinib) reversed the acute inhibitory effect of EGF on chloride secretion induced by carbachol (CCh) across T84 human colonic epithelial cells, which correlated with the diarrhea-inducing effect of each agent clinically. Carbachol 134-143 epidermal growth factor receptor Homo sapiens 0-4 32652816-3 2020 EGFr TKIs (such as afatinib, erlotinib, and osimertinib) reversed the acute inhibitory effect of EGF on chloride secretion induced by carbachol (CCh) across T84 human colonic epithelial cells, which correlated with the diarrhea-inducing effect of each agent clinically. Carbachol 145-148 epidermal growth factor receptor Homo sapiens 0-4 32652816-5 2020 Furthermore, afatinib and erlotinib prevented EGF- or CCh-induced EGFr phosphorylation. Carbachol 54-57 epidermal growth factor receptor Homo sapiens 66-70 32652816-6 2020 EGFr TKIs also suppressed phosphorylation of extracellular signal-regulated kinase (Erk)1/2 in response to EGF, whereas they had weaker effects on CCh-induced Erk1/2 phosphorylation. Carbachol 147-150 epidermal growth factor receptor Homo sapiens 0-4 32652816-9 2020 CCh-activated Erk1/2 phosphorylation was relatively insensitive to EGFr TKIs and delayed the deleterious effects of EGFr TKIs on barrier function. Carbachol 0-3 epidermal growth factor receptor Homo sapiens 116-120