摘要
Tribbles相关蛋白(TRB)家族成员是哺乳动物果蝇Tribbles的同源基因。Tribbles原本被认为是在果蝇的发育过程中一个细胞周期调节器。Tribbles基因在进化上是保守的,并且三个TRB基因(TRB1、TRB2 和TRB3)已确定存在于哺乳动物中。TRBs是假激酶,因为他们缺乏一种对激酶活性作用的ATP结合位点或一种重要的保守催化基序。相反,在各种细胞过程中扮演重要的角色,如作为支架或适配器促进靶蛋白的降解和规范几个关键的信号转导途径。最近的研究集中在TRBs在肿瘤发生和肿瘤进展的作用。在本篇综述中,我们重点研究TRB家族成员通过泛素-蛋白酶体系统的调节在肿瘤发生中的生理作用,和讨论TRBs作为癌症生物标志物和潜在的治疗靶点。
关键词: 引起白血病,致癌基因,TRB1,TRB2,TRB3,肿瘤发生,泛素-蛋白酶体系统。
Current Cancer Drug Targets
Title:Tribbles-Related Protein Family Members as Regulators or Substrates of the Ubiquitin-Proteasome System in Cancer Development
Volume: 16 Issue: 2
Author(s): Satoshi Sakai, Chiharu Miyajima, Chiharu Uchida, Yuka Itoh, Hidetoshi Hayashi and Yasumichi Inoue
Affiliation:
关键词: 引起白血病,致癌基因,TRB1,TRB2,TRB3,肿瘤发生,泛素-蛋白酶体系统。
摘要: Tribbles-related protein (TRB) family members are the mammalian orthologs of Drosophila tribbles. Tribbles was originally identified as a cell cycle regulator during Drosophila development. Tribbles genes are evolutionary conserved, and three TRB genes (TRB1, TRB2 and TRB3) have been identified in mammals. TRBs are considered pseudokinases because they lack an ATP binding site or one of the conserved catalytic motifs essential for kinase activity. Instead, TRBs play important roles in various cellular processes as scaffolds or adaptors to promote the degradation of target proteins and to regulate several key signaling pathways. Recent research has focused on the role of TRBs in tumorigenesis and neoplastic progression. In this review, we focus on the physiological roles of TRB family members in tumorigenesis through the regulation of the ubiquitin-proteasome system and discuss TRBs as biomarkers or potential therapeutic targets in cancer.
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Cite this article as:
Satoshi Sakai, Chiharu Miyajima, Chiharu Uchida, Yuka Itoh, Hidetoshi Hayashi and Yasumichi Inoue , Tribbles-Related Protein Family Members as Regulators or Substrates of the Ubiquitin-Proteasome System in Cancer Development, Current Cancer Drug Targets 2016; 16 (2) . https://dx.doi.org/10.2174/1568009616666151112122645
DOI https://dx.doi.org/10.2174/1568009616666151112122645 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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