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本文引用的文献

1
How common are extraribosomal functions of ribosomal proteins?核糖体蛋白的核糖体外功能有多常见?
Mol Cell. 2009 Apr 10;34(1):3-11. doi: 10.1016/j.molcel.2009.03.006.
2
The p53 tumor suppressor causes congenital malformations in Rpl24-deficient mice and promotes their survival.p53肿瘤抑制因子在Rpl24基因缺陷型小鼠中会引发先天性畸形,并提高其存活率。
Mol Cell Biol. 2009 May;29(10):2489-504. doi: 10.1128/MCB.01588-08. Epub 2009 Mar 9.
3
Active-site inhibitors of mTOR target rapamycin-resistant outputs of mTORC1 and mTORC2.mTOR的活性位点抑制剂靶向mTORC1和mTORC2的雷帕霉素抗性输出。
PLoS Biol. 2009 Feb 10;7(2):e38. doi: 10.1371/journal.pbio.1000038.
4
Suppression of Myc oncogenic activity by ribosomal protein haploinsufficiency.核糖体蛋白单倍剂量不足对Myc致癌活性的抑制作用。
Nature. 2008 Dec 18;456(7224):971-5. doi: 10.1038/nature07449. Epub 2008 Nov 16.
5
CDK11(p58) is required for the maintenance of sister chromatid cohesion.细胞周期蛋白依赖性激酶11(p58)是维持姐妹染色单体黏连所必需的。
J Cell Sci. 2007 Jul 15;120(Pt 14):2424-34. doi: 10.1242/jcs.007963.
6
Ablation of ribosomal protein L22 selectively impairs alphabeta T cell development by activation of a p53-dependent checkpoint.核糖体蛋白L22的缺失通过激活p53依赖的检查点选择性地损害αβ T细胞发育。
Immunity. 2007 Jun;26(6):759-72. doi: 10.1016/j.immuni.2007.04.012. Epub 2007 Jun 7.
7
14-3-3sigma controls mitotic translation to facilitate cytokinesis.14-3-3σ蛋白控制有丝分裂期翻译以促进胞质分裂。
Nature. 2007 Mar 15;446(7133):329-32. doi: 10.1038/nature05584.
8
Ribosomal protein S6 gene haploinsufficiency is associated with activation of a p53-dependent checkpoint during gastrulation.核糖体蛋白S6基因单倍剂量不足与原肠胚形成过程中p53依赖的检查点激活有关。
Mol Cell Biol. 2006 Dec;26(23):8880-91. doi: 10.1128/MCB.00751-06. Epub 2006 Sep 25.
9
The c-Myc target gene network.c-Myc靶基因网络。
Semin Cancer Biol. 2006 Aug;16(4):253-64. doi: 10.1016/j.semcancer.2006.07.014. Epub 2006 Jul 25.
10
Activation by c-Myc of transcription by RNA polymerases I, II and III.c-Myc对RNA聚合酶I、II和III转录的激活作用。
Biochem Soc Symp. 2006(73):141-54. doi: 10.1042/bss0730141.

Myc诱导的蛋白质合成在癌症中的作用。

The role of Myc-induced protein synthesis in cancer.

作者信息

Ruggero Davide

机构信息

School of Medicine and Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 94158, USA.

出版信息

Cancer Res. 2009 Dec 1;69(23):8839-43. doi: 10.1158/0008-5472.CAN-09-1970. Epub 2009 Nov 24.

DOI:10.1158/0008-5472.CAN-09-1970
PMID:19934336
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2880919/
Abstract

Deregulation in different steps of translational control is an emerging mechanism for cancer formation. One example of an oncogene with a direct role in control of translation is the Myc transcription factor. Myc directly increases protein synthesis rates by controlling the expression of multiple components of the protein synthetic machinery, including ribosomal proteins and initiation factors of translation, Pol III and rDNA. However, the contribution of Myc-dependent increases in protein synthesis toward the multistep process leading to cancer has remained unknown. Recent evidence strongly suggests that Myc oncogenic signaling may monopolize the translational machinery to elicit cooperative effects on cell growth, cell cycle progression, and genome instability as a mechanism for cancer initiation. Moreover, new genetic tools to restore aberrant increases in protein synthesis control are now available, which should enable the dissection of important mechanisms in cancer that rely on the translational machinery.

摘要

翻译控制不同步骤中的失调是癌症形成的一种新兴机制。在翻译控制中具有直接作用的一个癌基因实例是Myc转录因子。Myc通过控制蛋白质合成机制的多个组分的表达,包括核糖体蛋白、翻译起始因子、Pol III和rDNA,直接提高蛋白质合成速率。然而,Myc依赖性的蛋白质合成增加对导致癌症的多步骤过程的贡献仍不清楚。最近的证据有力地表明,Myc致癌信号可能垄断翻译机制,以引发对细胞生长、细胞周期进程和基因组不稳定的协同作用,作为癌症起始的一种机制。此外,现在有了恢复蛋白质合成控制异常增加的新遗传工具,这应该能够剖析癌症中依赖翻译机制的重要机制。