癌症中的蛋白激酶药物:从小分子到纳米颗粒

Devan, G. Venkatasubbu
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引用次数: 0

摘要

中国生物医学工程学报,2017,35(5):557 - 557。激酶活性失调是疾病的常见原因,特别是癌症,它们调节肿瘤进展和转移的许多重要方面。在一些情况下,蛋白激酶通过磷酸化个体发生和肿瘤抑制蛋白来调节癌症的进展,从而调节活性、稳定性和功能[4-8]。有趣的是,目前发现的许多肿瘤抑制基因和显性癌基因也是蛋白激酶。c-Src、c-Abl、丝裂原活化蛋白(MAP)激酶、磷脂酰肌醇-3-激酶(PI3K) AKT和表皮生长因子(EGF)受体等激酶在癌细胞中通常被激活,并参与肿瘤发生[9-13]。鉴于蛋白激酶在癌症等人类疾病中的重要性,它们已成为有吸引力的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Drugging protein kinases in cancer: from small molecules to nanoparticles
MOJ Proteomics Bioinform 2017, 5(5): 00173 upstream protein kinase. Deregulated kinase activity is a frequent cause of disease, particularly cancer, where they regulate many aspects important in tumor progression and metastasis. In several instances protein kinases regulates cancer progression by phosphorylating ontogenesis and tumor suppressor proteins thereby regulating the activity, stability, and function [4-8]. Interestingly, many of the tumor suppressor genes and dominant oncogenes identified so far are also protein kinases. Kinases such as c-Src, c-Abl, mitogen activated protein (MAP) kinase, phosphotidylinositol-3-kinase (PI3K) AKT, and the epidermal growth factor (EGF) receptor are commonly activated in cancer cells, and are known to contribute to tumor genesis [9-13].Given their importance in human diseases such as cancer, protein kinases have emerged as attractive therapeutic targets.
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