TAILIEUCHUNG - Báo cáo khoa học: The impact of the regulatory design on the response of epidermal growth factor receptor-mediated signal transduction towards oncogenic mutations

Epidermal growth factor receptor (EGFR)-mediated signal transduction is often hyperactivated in tumour cells and therefore considered a promising target for cancer therapy. A number of computational models have been developed which describe the pathway in great detail. | ỊFEBS Journal The impact of the regulatory design on the response of epidermal growth factor receptor-mediated signal transduction towards oncogenic mutations Jana Wolf 1 Serge Dronov 1 Frank Tobin2 and Igor Goryanin1 1 Scientific Computing and MathematicalModelling GlaxoSmithKline Medicines Research Centre Stevenage UK 2 Scientific Computing and MathematicalModelling GlaxoSmithKline King of Prussia PA USA Keywords cancer mathematicalmodel Ras mutations receptor overexpression robustness Correspondence J. Wolf TheoreticalBiophysics Institute of Biology Humboldt-University Invalidenstr. 42 10115 Berlin Germany Fax 49 30 20938813 Tel 49 30 20938382 E-mail Website http theorybp Present address TheoreticalBiophysics Institute of Biology Humboldt-University Berlin Germany fiThe University of Edinburgh UK Database The mathematical model described here has been submitted to the Online Cellular Systems Modelling Database and can be accessed free of charge at http . database wolf2 Received 10 June 2007 revised 10 August 2007 accepted 24 August 2007 doi Epidermal growth factor receptor EGFR -mediated signal transduction is often hyperactivated in tumour cells and therefore considered a promising target for cancer therapy. A number of computational models have been developed which describe the pathway in great detail. These models are similar in their description of the activation events. The deactivation of the EGFR signalling seems to be cell type-specific and is less understood. Deactivation via receptor internalization feedback inhibition of son of sevenless SOS by double phosphorylated extracellular signal-regulated kinase ERKPP or transiently activated Ras-GTPase activating protein Ras-GAP proteins is discussed to play a role. In this study we address the question of to what extent the effect of oncogenic perturbations on EGFR signalling depend on the

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