ArticleMolecular and cellular biology1999
Bradykinin B(2) receptor-mediated mitogen-activated protein kinase activation in COS-7 cells requires dual signaling via both protein kinase C pathway and epidermal growth factor receptor transactivation.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 106 citations in OpenAlex.
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- Cancer progression in COVID-19: integrating the roles of renin angiotensin aldosterone system, angiopoietin-2, heat shock protein-27 and epithelial mesenchymal transition.Ecancermedicalscience · 2020Article
- Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Anti-inflammatory mechanism of polyunsaturated fatty acids in Helicobacter pylori-infected gastric epithelial cells.Mediators of inflammation · 2014Article
- Endothelial nitric-oxide synthase activation generates an inducible nitric-oxide synthase-like output of nitric oxide in inflamed endothelium.The Journal of biological chemistry · 2013Article
- Article
- Antitumor mechanisms of targeting the PDK1 pathway in head and neck cancer.Molecular cancer therapeutics · 2012Article
- The bradykinin B(2) receptor induces multiple cellular responses leading to the proliferation of human renal carcinoma cell lines.Cancer management and research · 2012Article
- Thrombospondin-1 opens the paracellular pathway in pulmonary microvascular endothelia through EGFR/ErbB2 activation.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Protein kinase C regulates the internalization and function of the human organic anion transporting polypeptide 1A2.British journal of pharmacology · 2011Article
- Beta-arrestin 2 is required for B1 receptor-dependent post-translational activation of inducible nitric oxide synthase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Differential regulation of inducible and endothelial nitric oxide synthase by kinin B1 and B2 receptors.Neuropeptides · 2010Review
- Phosphorylation of the mu-opioid receptor at tyrosine 166 (Tyr3.51) in the DRY motif reduces agonist efficacy.Molecular pharmacology · 2010Article
- The counteradhesive proteins, thrombospondin 1 and SPARC/osteonectin, open the tyrosine phosphorylation-responsive paracellular pathway in pulmonary vascular endothelia.Microvascular research · 2009Review
- Simvastatin reverses cardiac hypertrophy caused by disruption of the bradykinin 2 receptor.Canadian journal of physiology and pharmacology · 2008Article
- Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathways.Journal of molecular and cellular cardiology · 2007Article
- Mechanisms of endothelin-1-induced MAP kinase activation in adrenal glomerulosa cells.The Journal of steroid biochemistry and molecular biology · 2006Article
- Regulation of ERK1/2 activity by ghrelin-activated growth hormone secretagogue receptor 1A involves a PLC/PKCvarepsilon pathway.British journal of pharmacology · 2006Article
- Potentiation of bradykinin actions by analogues of the bradykinin potentiating nonapeptide BPP9alpha.Peptides · 2005Article
- Site-selective regulation of platelet-derived growth factor beta receptor tyrosine phosphorylation by T-cell protein tyrosine phosphatase.Molecular and cellular biology · 2004Article
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The signaling routes linking G-protein-coupled receptors to mitogen-activated protein kinase (MAPK) may involve tyrosine kinases, phosphoinositide 3-kinase gamma (PI3Kgamma), and protein kinase C (PKC). To characterize the mitogenic pathway of bradykinin (BK), COS-7 cells were transiently cotransfected with the human bradykinin B(2) receptor and hemagglutinin-tagged MAPK. We demonstrate that BK-induced activation of MAPK is mediated via the alpha subunits of a G(q/11) protein. Both activation of Raf-1 and activation of MAPK in response to BK were blocked by inhibitors of PKC as well as of the epidermal growth factor (EGF) receptor. Furthermore, in PKC-depleted COS-7 cells, the effect of BK on MAPK was clearly reduced. Inhibition of PI3-Kgamma or Src kinase failed to diminish MAPK activation by BK. BK-induced translocation and overexpression of PKC isoforms as well as coexpression of inactive or constitutively active mutants of different PKC isozymes provided evidence for a role of the diacylglycerol-sensitive PKCs alpha and epsilon in BK signaling toward MAPK. In addition to PKC activation, BK also induced tyrosine phosphorylation of EGF receptor (transactivation) in COS-7 cells. Inhibition of PKC did not alter BK-induced transactivation, and blockade of EGF receptor did not affect BK-stimulated phosphatidylinositol turnover or BK-induced PKC translocation, suggesting that PKC acts neither upstream nor downstream of the EGF receptor. Comparison of the kinetics of PKC activation and EGF receptor transactivation in response to BK also suggests simultaneous rather than consecutive signaling. We conclude that in COS-7 cells, BK activates MAPK via a permanent dual signaling pathway involving the independent activation of the PKC isoforms alpha and epsilon and transactivation of the EGF receptor. The two branches of this pathway may converge at the level of the Ras-Raf complex.
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