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It is known that the cancer cells rapidly proliferate, as the epidermal growth factor receptor (EGFR) is overexpressed on the cell surface. EGFR is a tyrosine kinase receptor and by binding the epidermal growth factor (EGF) certain proteins are activated which will provide dimerization. Many treatment modalities and drugs have been developed to inhibit proliferation. Some of these drugs target the external region of EGFR, which is the binding site for EGF. In some cases, drug resistance is developed resulting in ineffective treatment. The aim of this study is to design a system to demonstrate physicochemical and structural differences between wild type and mutant EGFR by generating EGFRs containing mutations that provide resistance to drugs to overcome the resistance problem. This system uses EGFR mRNA as a template and expresses wild type and mutant EGFR in CHO cells to demonstrate the effect of physicochemical and structural differences on the interaction between EGF and EGFR.
机译:众所周知,由于表皮生长因子受体(EGFR)在细胞表面过度表达,癌细胞会迅速增殖。 EGFR是酪氨酸激酶受体,通过结合表皮生长因子(EGF),某些蛋白质被激活,从而提供二聚作用。已经开发了许多治疗方式和药物来抑制增殖。这些药物中有一些靶向EGFR的外部区域,该区域是EGF的结合位点。在某些情况下,会产生耐药性,导致治疗无效。这项研究的目的是设计一个系统,通过产生包含对药物产生抗性以克服耐药性问题的突变的EGFR,来证明野生型和突变型EGFR之间的理化和结构差异。该系统以EGFR mRNA为模板,并在CHO细胞中表达野生型和突变型EGFR,以证明理化和结构差异对EGF与EGFR相互作用的影响。

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