• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

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

千面蛋白:p53的肿瘤抑制与致癌反应

Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.

作者信息

Marques Mayra A, de Andrade Guilherme C, Silva Jerson L, de Oliveira Guilherme A P

机构信息

Institute of Medical Biochemistry Leopoldo de Meis, National Institute of Science and Technology for Structural Biology and Bioimaging, National Center of Nuclear Magnetic Resonance Jiri Jonas, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

出版信息

Front Mol Biosci. 2022 Aug 25;9:944955. doi: 10.3389/fmolb.2022.944955. eCollection 2022.

DOI:10.3389/fmolb.2022.944955
PMID:36090037
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9452956/
Abstract

The p53 protein is a pleiotropic regulator working as a tumor suppressor and as an oncogene. Depending on the cellular insult and the mutational status, p53 may trigger opposing activities such as cell death or survival, senescence and cell cycle arrest or proliferative signals, antioxidant or prooxidant activation, glycolysis, or oxidative phosphorylation, among others. By augmenting or repressing specific target genes or directly interacting with cellular partners, p53 accomplishes a particular set of activities. The mechanism in which p53 is activated depends on increased stability through post-translational modifications (PTMs) and the formation of higher-order structures (HOS). The intricate cell death and metabolic p53 response are reviewed in light of gaining stability PTM and HOS formation in health and disease.

摘要

p53蛋白是一种多效调节剂,兼具肿瘤抑制因子和癌基因的作用。根据细胞所受损伤及突变状态,p53可能引发相反的活动,如细胞死亡或存活、衰老、细胞周期停滞或增殖信号、抗氧化或促氧化激活、糖酵解或氧化磷酸化等。通过增强或抑制特定靶基因或直接与细胞伴侣相互作用,p53实现了一系列特定的活动。p53被激活的机制取决于通过翻译后修饰(PTM)增加稳定性以及高阶结构(HOS)的形成。鉴于在健康和疾病状态下稳定性的获得、PTM和HOS的形成,对复杂的细胞死亡和代谢性p53反应进行了综述。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/2c4214b9e518/fmolb-09-944955-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/2c486ca90192/fmolb-09-944955-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/3c5a595aabbb/fmolb-09-944955-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/e26b97f556d8/fmolb-09-944955-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/2c4214b9e518/fmolb-09-944955-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/2c486ca90192/fmolb-09-944955-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/3c5a595aabbb/fmolb-09-944955-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/e26b97f556d8/fmolb-09-944955-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ff4/9452956/2c4214b9e518/fmolb-09-944955-g004.jpg

相似文献

1
Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.千面蛋白:p53的肿瘤抑制与致癌反应
Front Mol Biosci. 2022 Aug 25;9:944955. doi: 10.3389/fmolb.2022.944955. eCollection 2022.
2
Deciphering the PTM codes of the tumor suppressor p53.解析肿瘤抑制因子 p53 的 PTM 密码。
J Mol Cell Biol. 2022 Jan 21;13(11):774-785. doi: 10.1093/jmcb/mjab047.
3
Oncogenic ras and p53 cooperate to induce cellular senescence.致癌性Ras和p53协同作用诱导细胞衰老。
Mol Cell Biol. 2002 May;22(10):3497-508. doi: 10.1128/MCB.22.10.3497-3508.2002.
4
TRIM8 modulates p53 activity to dictate cell cycle arrest.TRIM8 通过调节 p53 活性来决定细胞周期停滞。
Cell Cycle. 2012 Feb 1;11(3):511-23. doi: 10.4161/cc.11.3.19008.
5
The p53 transcriptional response across tumor types reveals core and senescence-specific signatures modulated by long noncoding RNAs.肿瘤类型中 p53 转录反应揭示了受长非编码 RNA 调控的核心和衰老特异性特征。
Proc Natl Acad Sci U S A. 2021 Aug 3;118(31). doi: 10.1073/pnas.2025539118.
6
A new twist in the feedback loop: stress-activated MDM2 destabilization is required for p53 activation.反馈回路中的一个新转折:p53激活需要应激激活的MDM2去稳定化。
Cell Cycle. 2005 Mar;4(3):411-7. doi: 10.4161/cc.4.3.1522. Epub 2005 Mar 2.
7
The regulation of cellular metabolism by tumor suppressor p53.肿瘤抑制因子 p53 对细胞代谢的调节。
Cell Biosci. 2013 Feb 6;3(1):9. doi: 10.1186/2045-3701-3-9.
8
PML regulates p53 acetylation and premature senescence induced by oncogenic Ras.早幼粒细胞白血病蛋白(PML)调控由致癌性Ras诱导的p53乙酰化和早衰。
Nature. 2000 Jul 13;406(6792):207-10. doi: 10.1038/35018127.
9
p53, oxidative stress, and aging.p53、氧化应激与衰老。
Antioxid Redox Signal. 2011 Sep 15;15(6):1669-78. doi: 10.1089/ars.2010.3644. Epub 2011 Feb 7.
10
Mitochondrial death functions of p53.p53的线粒体死亡功能
Mol Cell Oncol. 2014 Oct 31;1(2):e955995. doi: 10.1080/23723548.2014.955995. eCollection 2014 Apr-Jun.

引用本文的文献

1
Current insights into the oncogenic roles of lncRNA LINC00355.lncRNA LINC00355致癌作用的当前见解。
Cancer Innov. 2023 Sep 14;2(6):448-462. doi: 10.1002/cai2.91. eCollection 2023 Dec.
2
p53 amyloid pathology is correlated with higher cancer grade irrespective of the mutant or wild-type form.p53 淀粉样蛋白病理学与更高的癌症分级相关,而与突变型或野生型形式无关。
J Cell Sci. 2023 Sep 1;136(17). doi: 10.1242/jcs.261017. Epub 2023 Sep 8.
3
LSD1 promotes prostate cancer reprogramming by repressing TP53 signaling independently of its demethylase function.

本文引用的文献

1
Relevance of Amorphous and Amyloid-Like Aggregates of the p53 Core Domain to Loss of its DNA-Binding Activity.p53核心结构域的无定形和淀粉样聚集体与其DNA结合活性丧失的相关性。
Front Mol Biosci. 2022 Apr 26;9:869851. doi: 10.3389/fmolb.2022.869851. eCollection 2022.
2
NMR methods for exploring 'dark' states in ligand binding and protein-protein interactions.NMR 方法在配体结合和蛋白质-蛋白质相互作用中探索“暗”状态。
Prog Nucl Magn Reson Spectrosc. 2022 Feb;128:1-24. doi: 10.1016/j.pnmrs.2021.10.001. Epub 2021 Nov 2.
3
Nucleic acid actions on abnormal protein aggregation, phase transitions and phase separation.
LSD1 通过抑制 TP53 信号通路来促进前列腺癌重编程,而不依赖其去甲基化酶功能。
JCI Insight. 2023 Aug 8;8(15):e167440. doi: 10.1172/jci.insight.167440.
4
Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy.肝细胞癌的发病机制:细胞凋亡与自噬的相互作用
Biomedicines. 2023 Apr 13;11(4):1166. doi: 10.3390/biomedicines11041166.
5
Therapeutic Targeting of P53: A Comparative Analysis of APR-246 and COTI-2 in Human Tumor Primary Culture 3-D Explants.APR-246 和 COTI-2 对人源肿瘤原代培养 3-D 外植体的治疗靶点比较分析
Genes (Basel). 2023 Mar 19;14(3):747. doi: 10.3390/genes14030747.
核酸对异常蛋白质聚集、相变和相分离的作用。
Curr Opin Struct Biol. 2022 Apr;73:102346. doi: 10.1016/j.sbi.2022.102346. Epub 2022 Mar 2.
4
The Cross Talk Between p53 and mTOR Pathways in Response to Physiological and Genotoxic Stresses.p53与mTOR信号通路在应对生理应激和基因毒性应激时的相互作用
Front Cell Dev Biol. 2021 Nov 18;9:775507. doi: 10.3389/fcell.2021.775507. eCollection 2021.
5
Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.p53 介导的细胞对 DNA 损伤治疗药物的反应差异。
Int J Mol Sci. 2021 Oct 31;22(21):11828. doi: 10.3390/ijms222111828.
6
Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells.Δ133p53β 异构体的促侵袭活性通过癌细胞中的聚集依赖性机制进行调节。
Nat Commun. 2021 Sep 15;12(1):5463. doi: 10.1038/s41467-021-25550-2.
7
Deciphering the PTM codes of the tumor suppressor p53.解析肿瘤抑制因子 p53 的 PTM 密码。
J Mol Cell Biol. 2022 Jan 21;13(11):774-785. doi: 10.1093/jmcb/mjab047.
8
The E3 Ligase PIAS1 Regulates p53 Sumoylation to Control Stress-Induced Apoptosis of Lens Epithelial Cells Through the Proapoptotic Regulator Bax.E3泛素连接酶PIAS1通过促凋亡调节因子Bax调控p53的SUMO化,以控制应激诱导的晶状体上皮细胞凋亡。
Front Cell Dev Biol. 2021 Jun 14;9:660494. doi: 10.3389/fcell.2021.660494. eCollection 2021.
9
Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function.蛋白质模拟淀粉样蛋白抑制剂可有效消除癌症相关的突变型p53聚集并恢复肿瘤抑制功能。
Nat Commun. 2021 Jun 25;12(1):3962. doi: 10.1038/s41467-021-23985-1.
10
Phase separation of p53 precedes aggregation and is affected by oncogenic mutations and ligands.p53的相分离先于聚集,并受致癌突变和配体的影响。
Chem Sci. 2021 Apr 26;12(21):7334-7349. doi: 10.1039/d1sc01739j.