• 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

Selective degradation of the p53-R175H oncogenic hotspot mutant by an RNA aptamer-based PROTAC.

作者信息

Kong Lingping, Meng Fanlu, Wu Sijin, Zhou Ping, Ge Ruixin, Liu Min, Zhang Linlin, Zhou Jun, Zhong Diansheng, Xie Songbo

机构信息

Department of Medical Oncology, Tianjin Medical University General Hospital, Tianjin, China.

Laboratory of Molecular Modeling and Design, State Key Laboratory of Molecular Reaction Dynamics, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.

出版信息

Clin Transl Med. 2023 Feb;13(2):e1191. doi: 10.1002/ctm2.1191.

DOI:10.1002/ctm2.1191
PMID:36710401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9884801/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/2df41b963612/CTM2-13-e1191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/cb7a7e8a1788/CTM2-13-e1191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/66f6adcf65f0/CTM2-13-e1191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/2df41b963612/CTM2-13-e1191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/cb7a7e8a1788/CTM2-13-e1191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/66f6adcf65f0/CTM2-13-e1191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5640/9884801/2df41b963612/CTM2-13-e1191-g001.jpg

相似文献

1
Selective degradation of the p53-R175H oncogenic hotspot mutant by an RNA aptamer-based PROTAC.基于RNA适配体的PROTAC对p53-R175H致癌热点突变体的选择性降解
Clin Transl Med. 2023 Feb;13(2):e1191. doi: 10.1002/ctm2.1191.
2
An engineered DNA aptamer-based PROTAC for precise therapy of p53-R175H hotspot mutant-driven cancer.一种基于工程化 DNA 适体的 PROTAC,用于精准治疗 p53-R175H 热点突变驱动的癌症。
Sci Bull (Beijing). 2024 Jul 15;69(13):2122-2135. doi: 10.1016/j.scib.2024.05.017. Epub 2024 May 18.
3
Elevated expression of p53 gain-of-function mutation R175H in endometrial cancer cells can increase the invasive phenotypes by activation of the EGFR/PI3K/AKT pathway.子宫内膜癌细胞中 p53 功能获得性突变 R175H 的高表达可通过激活 EGFR/PI3K/AKT 通路增加侵袭表型。
Mol Cancer. 2009 Nov 16;8:103. doi: 10.1186/1476-4598-8-103.
4
The isolation of an RNA aptamer targeting to p53 protein with single amino acid mutation.靶向具有单氨基酸突变的p53蛋白的RNA适配体的分离。
Proc Natl Acad Sci U S A. 2015 Aug 11;112(32):10002-7. doi: 10.1073/pnas.1502159112. Epub 2015 Jul 27.
5
Mutant p53(R175H) upregulates Twist1 expression and promotes epithelial-mesenchymal transition in immortalized prostate cells.突变型 p53(R175H)上调 Twist1 表达并促进永生化前列腺细胞的上皮间质转化。
Cell Death Differ. 2011 Feb;18(2):271-81. doi: 10.1038/cdd.2010.94. Epub 2010 Aug 6.
6
The gain of function of p53 cancer mutant in promoting mammary tumorigenesis.p53 癌突变促进乳腺肿瘤发生的功能获得。
Oncogene. 2013 Jun 6;32(23):2900-6. doi: 10.1038/onc.2012.299. Epub 2012 Jul 23.
7
Colletofragarone A2 Inhibits Cancer Cell Growth and Leads to the Degradation and Aggregation of Mutant p53.A2 型胶原酶抑制癌细胞生长并导致突变型 p53 的降解和聚集。
Chem Res Toxicol. 2022 Sep 19;35(9):1598-1603. doi: 10.1021/acs.chemrestox.2c00202. Epub 2022 Aug 26.
8
p53 mutant-type in human prostate cancer cells determines the sensitivity to phenethyl isothiocyanate induced growth inhibition.p53 突变型在人类前列腺癌细胞中决定了对苯乙基异硫氰酸酯诱导的生长抑制的敏感性。
J Exp Clin Cancer Res. 2019 Jul 15;38(1):307. doi: 10.1186/s13046-019-1267-z.
9
DN-R175H p53 mutation is more effective than p53 interference in inducing epithelial disorganization and activation of proliferation signals in human carcinoma cells: role of E-cadherin.DN-R175H p53突变在诱导人癌细胞上皮组织紊乱和增殖信号激活方面比p53干扰更有效:E-钙黏蛋白的作用
Int J Cancer. 2009 Oct 1;125(7):1604-12. doi: 10.1002/ijc.24512.
10
Mutant p53 promotes cancer initiation in the pancreas by stabilizing HSP70.突变型 p53 通过稳定 HSP70 促进胰腺中的癌症发生。
Cancer Lett. 2019 Jul 1;453:122-130. doi: 10.1016/j.canlet.2019.03.047. Epub 2019 Apr 1.

引用本文的文献

1
Unraveling the secrets of novel PROTACs to improve degradation efficacy.揭开新型蛋白降解靶向嵌合体(PROTACs)的秘密以提高降解效率。
Mol Divers. 2025 Jul 5. doi: 10.1007/s11030-025-11273-9.
2
Discovery of Drugs Targeting Mutant p53 and Progress in Nano-Enabled Therapeutic Strategy for p53-Mutated Cancers.靶向突变型p53的药物发现及p53突变型癌症的纳米治疗策略进展
Biomolecules. 2025 May 26;15(6):763. doi: 10.3390/biom15060763.
3
Identification of a non-inhibitory aptameric ligand to CRL2 E3 ligase for targeted protein degradation.

本文引用的文献

1
Inducible Degradation of Oncogenic Nucleolin Using an Aptamer-Based PROTAC.基于适体的 PROTAC 诱导致癌核仁蛋白降解
J Med Chem. 2023 Jan 26;66(2):1339-1348. doi: 10.1021/acs.jmedchem.2c01557. Epub 2023 Jan 6.
2
Development of a novel PROTAC using the nucleic acid aptamer as a targeting ligand for tumor selective degradation of nucleolin.一种新型PROTAC的开发,该PROTAC使用核酸适配体作为靶向配体,用于肿瘤选择性降解核仁素。
Mol Ther Nucleic Acids. 2022 Sep 19;30:66-79. doi: 10.1016/j.omtn.2022.09.008. eCollection 2022 Dec 13.
3
Chemistries of bifunctional PROTAC degraders.
鉴定一种靶向蛋白降解的CRL2 E3连接酶非抑制性适体配体。
Nat Commun. 2025 Mar 13;16(1):2494. doi: 10.1038/s41467-025-57823-5.
4
Decoding the functional impact of the cancer genome through protein-protein interactions.通过蛋白质-蛋白质相互作用解码癌症基因组的功能影响。
Nat Rev Cancer. 2025 Mar;25(3):189-208. doi: 10.1038/s41568-024-00784-6. Epub 2025 Jan 14.
5
Promising Proteolysis-Targeting Chimera for Mutant p53-R175H.针对突变型p53-R175H的有前景的蛋白酶靶向嵌合体
ACS Omega. 2024 Nov 1;9(45):45138-45146. doi: 10.1021/acsomega.4c06177. eCollection 2024 Nov 12.
6
Targeted protein degradation: advances in drug discovery and clinical practice.靶向蛋白降解:药物发现和临床实践的进展。
Signal Transduct Target Ther. 2024 Nov 6;9(1):308. doi: 10.1038/s41392-024-02004-x.
7
The significant others of aurora kinase a in cancer: combination is the key.极光激酶A在癌症中的重要关联因素:联合治疗是关键。
Biomark Res. 2024 Sep 27;12(1):109. doi: 10.1186/s40364-024-00651-4.
8
CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.CYLD/HDAC6 信号通路调控肺纤维化过程中上皮-间充质转化与纤毛动态平衡的相互作用。
Cell Death Dis. 2024 Aug 9;15(8):581. doi: 10.1038/s41419-024-06972-4.
9
Targeted degradation of membrane and extracellular proteins with LYTACs.利用LYTACs对膜蛋白和细胞外蛋白进行靶向降解。
Acta Pharmacol Sin. 2025 Jan;46(1):1-7. doi: 10.1038/s41401-024-01364-y. Epub 2024 Aug 5.
10
Antitumor Effect of Anti-c-Myc Aptamer-Based PROTAC for Degradation of the c-Myc Protein.基于抗 c-Myc 适体的 PROTAC 降解 c-Myc 蛋白的抗肿瘤作用。
Adv Sci (Weinh). 2024 Jul;11(26):e2309639. doi: 10.1002/advs.202309639. Epub 2024 Apr 29.
双功能 PROTAC 降解剂的化学。
Chem Soc Rev. 2022 Aug 15;51(16):7066-7114. doi: 10.1039/d2cs00220e.
4
Targeting Undruggable Transcription Factors with PROTACs: Advances and Perspectives.靶向不可成药转录因子的 PROTAC 技术:进展与展望。
J Med Chem. 2022 Aug 11;65(15):10183-10194. doi: 10.1021/acs.jmedchem.2c00691. Epub 2022 Jul 26.
5
Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?TP53 激活了许多细胞反应,其中哪些对肿瘤抑制至关重要?
Cell Death Differ. 2022 May;29(5):961-971. doi: 10.1038/s41418-022-00996-z. Epub 2022 Apr 8.
6
Mutant p53: it's not all one and the same.突变型 p53:并非千篇一律。
Cell Death Differ. 2022 May;29(5):983-987. doi: 10.1038/s41418-022-00989-y. Epub 2022 Mar 31.
7
The Function of the Mutant p53-R175H in Cancer.突变型p53-R175H在癌症中的作用
Cancers (Basel). 2021 Aug 13;13(16):4088. doi: 10.3390/cancers13164088.
8
Targeting a neoantigen derived from a common mutation.靶向一种常见突变衍生的新抗原。
Science. 2021 Mar 5;371(6533). doi: 10.1126/science.abc8697. Epub 2021 Mar 1.
9
The isolation of an RNA aptamer targeting to p53 protein with single amino acid mutation.靶向具有单氨基酸突变的p53蛋白的RNA适配体的分离。
Proc Natl Acad Sci U S A. 2015 Aug 11;112(32):10002-7. doi: 10.1073/pnas.1502159112. Epub 2015 Jul 27.