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本文引用的文献

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Development of Soft Tissue Sarcomas in Ribosomal Proteins L5 and S24 Heterozygous Mice.核糖体蛋白L5和S24杂合小鼠软组织肉瘤的发生
J Cancer. 2016 Jan 1;7(1):32-6. doi: 10.7150/jca.13292. eCollection 2016.
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Partial Loss of Rpl11 in Adult Mice Recapitulates Diamond-Blackfan Anemia and Promotes Lymphomagenesis.成年小鼠中Rpl11部分缺失重现了先天性纯红细胞再生障碍性贫血并促进淋巴瘤发生。
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Structure of human MDM2 complexed with RPL11 reveals the molecular basis of p53 activation.与RPL11复合的人MDM2结构揭示了p53激活的分子基础。
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Ribosomal Protein Mutations Result in Constitutive p53 Protein Degradation through Impairment of the AKT Pathway.核糖体蛋白突变通过损害AKT途径导致p53蛋白持续性降解。
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p53 in survival, death and metabolic health: a lifeguard with a licence to kill.p53 在生存、死亡和代谢健康中的作用:有杀人执照的救生员。
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Oncogenic c-Myc-induced lymphomagenesis is inhibited non-redundantly by the p19Arf-Mdm2-p53 and RP-Mdm2-p53 pathways.致癌性c-Myc诱导的淋巴瘤发生受到p19Arf-Mdm2-p53和RP-Mdm2-p53通路的非冗余抑制。
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Ribosomal proteins: functions beyond the ribosome.核糖体蛋白:核糖体之外的功能。
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8
Perturbation of ribosome biogenesis drives cells into senescence through 5S RNP-mediated p53 activation.核糖体生物发生的扰乱通过 5S RNP 介导的 p53 激活将细胞驱进入衰老。
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Ribosomopathies: mechanisms of disease.核糖体病:疾病机制
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Nucleolar stress with and without p53.伴有和不伴有p53的核仁应激
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核糖体蛋白-MDM2-p53信号通路:连接核糖体生物合成与肿瘤监测

RP-MDM2-p53 Pathway: Linking Ribosomal Biogenesis and Tumor Surveillance.

作者信息

Liu Yong, Deisenroth Chad, Zhang Yanping

机构信息

Department of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

The Hamner Institutes for Health Sciences, Institute for Chemical Safety Sciences, 6 Davis Drive, PO Box 12137, Research Triangle Park, NC 27709, USA.

出版信息

Trends Cancer. 2016 Apr;2(4):191-204. doi: 10.1016/j.trecan.2016.03.002. Epub 2016 Apr 4.

DOI:10.1016/j.trecan.2016.03.002
PMID:28741571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5531060/
Abstract

Ribosomal biogenesis is tightly associated with cellular activities, such as growth, proliferation, and cell cycle progression. Perturbations in ribosomal biogenesis can initiate so-called nucleolar stress. The process through which ribosomal proteins (RPs) transduce nucleolar stress signals via MDM2 to p53 has been described as a crucial tumor-suppression mechanism. In this review we focus on recent progress pertaining to the function and mechanism of RPs in association with the MDM2-p53 tumor-suppression network, and the potential implications this surveillance network has for cancer development.

摘要

核糖体生物合成与细胞活动紧密相关,如生长、增殖和细胞周期进程。核糖体生物合成的扰动可引发所谓的核仁应激。核糖体蛋白(RPs)通过MDM2将核仁应激信号转导至p53的过程已被描述为一种关键的肿瘤抑制机制。在本综述中,我们聚焦于核糖体蛋白在与MDM2-p53肿瘤抑制网络相关的功能和机制方面的最新进展,以及这个监测网络对癌症发展的潜在影响。