假激酶 SgK269 和 SgK223：人类癌症中的新型致癌联盟。
The pseudokinases SgK269 and SgK223: A novel oncogenic alliance in human cancer.
机构信息
a Cancer Program, Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology , Monash University , Melbourne , Victoria , Australia.
出版信息
Cell Adh Migr. 2018;12(6):524-528. doi: 10.1080/19336918.2017.1394570. Epub 2017 Dec 21.
Sugen kinases (SgK)269 (also known as PEAK1), and SgK223, an orthologue of rat pragmin and mouse NACK, are human pseudokinases that are implicated in the progression of several cancers. Both are scaffolding proteins that recruit distinct repertoires of signalling proteins and regulate a variety of biological endpoints including cell migration and invasion. To date, SgK269 and SgK223 have been largely studied as separate signalling entities. However, recent work has demonstrated that SgK269 and SgK223 undergo homo- and heterotypic association that determines signal output and biological response. Further characterization of the mechanism of action of these two pseudokinases will provide novel insights into how they promote cancer progression and may reveal novel therapeutic strategies. Here we review their structure, mechanism and function and roles they play in cancer pathogenesis.
苏根激酶（SgK）269（也称为 PEAK1）和 SgK223，大鼠 pragmin 和小鼠 NACK 的同源物，是涉及多种癌症进展的人类假激酶。它们都是支架蛋白，可募集不同的信号蛋白库，并调节多种生物学终点，包括细胞迁移和侵袭。迄今为止，SgK269 和 SgK223 主要作为独立的信号实体进行研究。然而，最近的工作表明，SgK269 和 SgK223 发生同型和异型缔合，从而决定信号输出和生物学反应。对这两种假激酶作用机制的进一步表征将为它们如何促进癌症进展提供新的见解，并可能揭示新的治疗策略。在这里，我们回顾它们的结构、机制和功能，以及它们在癌症发病机制中的作用。
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