Suppr超能文献

MB0和MBI是MYC中独立且不同的反式激活结构域,对细胞转化至关重要。

MB0 and MBI Are Independent and Distinct Transactivation Domains in MYC that Are Essential for Transformation.

作者信息

Zhang Qin, West-Osterfield Kimberly, Spears Erick, Li Zhaoliang, Panaccione Alexander, Hann Stephen R

机构信息

Department of Cell and Developmental Biology, Vanderbilt University, School of Medicine, 1121 21st Ave., Nashville, TN 37232, USA.

出版信息

Genes (Basel). 2017 May 6;8(5):134. doi: 10.3390/genes8050134.

Abstract

MYC is a transcription factor that is essential for cellular proliferation and development. Deregulation or overexpression of MYC occurs in a variety of human cancers. Ectopic expression of MYC causes hyperproliferation and transformation of cells in culture and tumorigenesis in several transgenic mouse models. Deregulation of MYC can also induce apoptosis through activation of p53 and/or ARF tumor suppressors as a safeguard to prevent tumorigenesis. MYC binds to thousands of genomic sites and regulates hundreds of target genes in a context-dependent fashion to mediate these diverse biological roles. The N-terminal region of MYC contains several conserved domains or MYC Boxes (MB), which influence the different MYC transcriptional and biological activities to varying degrees. However, the specific domains that mediate the ability of MYC to activate transcription remain ill defined. In this report, we have identified a new conserved transactivation domain (TAD), MB0, which is essential for MYC transactivation and target gene induction. We demonstrate that MB0 and MBI represent two distinct and independent TADs within the N-terminal 62 amino acids of MYC. In addition, both MB0 and MBI are essential for MYC transformation of primary fibroblasts in cooperation with activated RAS, while MB0 is necessary for efficient MYC-induced p53-independent apoptosis.

摘要

MYC是一种转录因子,对细胞增殖和发育至关重要。MYC的失调或过表达发生在多种人类癌症中。在几种转基因小鼠模型中,MYC的异位表达导致培养细胞的过度增殖和转化以及肿瘤发生。MYC的失调还可通过激活p53和/或ARF肿瘤抑制因子诱导细胞凋亡,作为预防肿瘤发生的一种保障机制。MYC与数千个基因组位点结合,并以上下文依赖的方式调节数百个靶基因,以介导这些不同的生物学作用。MYC的N端区域包含几个保守结构域或MYC框(MB),它们在不同程度上影响MYC的不同转录和生物学活性。然而,介导MYC激活转录能力的特定结构域仍不清楚。在本报告中,我们鉴定了一个新的保守反式激活结构域(TAD),即MB0,它对MYC反式激活和靶基因诱导至关重要。我们证明MB0和MBI代表MYC N端62个氨基酸内两个不同且独立的TAD。此外,MB0和MBI对于MYC与激活的RAS协同作用转化原代成纤维细胞都是必不可少的,而MB0是MYC诱导的不依赖p53的细胞凋亡所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4134/5448008/818147997174/genes-08-00134-g002.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验