AKT/PKB上下游调控因子及相关信号转导通路:进展性癌的分子通路

Abu Sayed, M. Hossain, Efaaj Islam, M. Asgar
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引用次数: 0

摘要

AKT或蛋白激酶B,丝氨酸/苏氨酸特异性蛋白激酶,在人和动物体内的细胞中有三种类似的同种异构体。AKT通过包括GPCR (G蛋白偶联受体)、RTK(受体酪氨酸激酶)、SYK(脾脏酪氨酸激酶)、JAK (Janus激酶)和RAS在内的多种上游调节因子被调节和激活,从而进一步激活多个协同下游级联。这些通路的失调影响细胞周期和细胞增殖,导致肿瘤的发生。因此,本研究旨在探索AKT的所有主要上行和下行调节因子以及相关的信号转导途径,作为通过靶向蛋白药物开发进一步详细研究或肿瘤或癌症临床管理的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Upstreaming and Downstreaming Regulators and associated signaling transduction pathways of AKT/PKB: A Molecular Gateway to Progressive Carcinoma
AKT or Protein Kinase B, the serine/threonine-specific protein kinase, is found in three analogous isoforms in cells of human and animal bodies. AKT is regulated and activated via various upstream regulators including GPCR (G protein-coupled receptor), RTK (Receptor tyrosine kinase), SYK (spleen tyrosine kinase), JAK (Janus kinase), and RAS lead to the further activation of multiple coordinated downstream cascades. The dysregulation of these pathways affects the cell cycle and cell proliferation, resulting in the development of carcinoma. Therefore, the study aimed with the objectives to explore all the major upstreaming and downstreaming regulators and associated signaling transduction pathways of AKT as an approach for further detailed studies or clinical management of tumors or cancers via targeted protein-based drug developments.
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