• 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

K63连接的泛素化在癌症中的作用。

Role of K63-linked ubiquitination in cancer.

作者信息

Cao Liangzi, Liu Xiaofang, Zheng Bowen, Xing Chengzhong, Liu Jingwei

机构信息

Department of Anus and Intestine Surgery, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.

出版信息

Cell Death Discov. 2022 Oct 6;8(1):410. doi: 10.1038/s41420-022-01204-0.

DOI:10.1038/s41420-022-01204-0
PMID:36202787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9537175/
Abstract

Ubiquitination is a critical type of post-translational modifications, of which K63-linked ubiquitination regulates interaction, translocation, and activation of proteins. In recent years, emerging evidence suggest involvement of K63-linked ubiquitination in multiple signaling pathways and various human diseases including cancer. Increasing number of studies indicated that K63-linked ubiquitination controls initiation, development, invasion, metastasis, and therapy of diverse cancers. Here, we summarized molecular mechanisms of K63-linked ubiquitination dictating different biological activities of tumor and highlighted novel opportunities for future therapy targeting certain regulation of K63-linked ubiquitination in tumor.

摘要

泛素化是一种关键的翻译后修饰类型,其中K63连接的泛素化调节蛋白质的相互作用、易位和激活。近年来,新出现的证据表明K63连接的泛素化参与多种信号通路以及包括癌症在内的各种人类疾病。越来越多的研究表明,K63连接的泛素化控制着多种癌症的起始、发展、侵袭、转移和治疗。在此,我们总结了K63连接的泛素化决定肿瘤不同生物学活性的分子机制,并强调了未来针对肿瘤中K63连接泛素化的特定调控进行治疗的新机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6919/9537175/d01f25b47e7b/41420_2022_1204_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6919/9537175/d01f25b47e7b/41420_2022_1204_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6919/9537175/d01f25b47e7b/41420_2022_1204_Fig1_HTML.jpg

相似文献

1
Role of K63-linked ubiquitination in cancer.K63连接的泛素化在癌症中的作用。
Cell Death Discov. 2022 Oct 6;8(1):410. doi: 10.1038/s41420-022-01204-0.
2
Novel Lys63-linked ubiquitination of IKKβ induces STAT3 signaling.新型IKKβ赖氨酸63连接的泛素化诱导STAT3信号传导。
Cell Cycle. 2014;13(24):3964-76. doi: 10.4161/15384101.2014.988026.
3
The role of K63-linked polyubiquitination in cardiac hypertrophy.K63 链接多泛素化在心脏肥大中的作用。
J Cell Mol Med. 2018 Oct;22(10):4558-4567. doi: 10.1111/jcmm.13669. Epub 2018 Aug 13.
4
Specific expression of k63-linked ubiquitination of calmodulin-like protein 5 in breast cancer of premenopausal patients.钙调蛋白样蛋白 5 的 K63 连接泛素化在绝经前患者乳腺癌中的特异性表达。
J Cancer Res Clin Oncol. 2013 Dec;139(12):2125-32. doi: 10.1007/s00432-013-1541-y. Epub 2013 Oct 22.
5
Oncogenic mutations in IKKβ function through global changes induced by K63-linked ubiquitination and result in autocrine stimulation.IKKβ 的致癌突变通过 K63 连接的泛素化诱导的全局变化发挥作用,并导致自分泌刺激。
PLoS One. 2018 Oct 18;13(10):e0206014. doi: 10.1371/journal.pone.0206014. eCollection 2018.
6
pVHL mediates K63-linked ubiquitination of IKKβ, leading to IKKβ inactivation.pVHL介导IKKβ的K63连接的泛素化,导致IKKβ失活。
Cancer Lett. 2016 Dec 1;383(1):1-8. doi: 10.1016/j.canlet.2016.09.009. Epub 2016 Sep 28.
7
TARBP2 inhibits IRF7 activation by suppressing TRAF6-mediated K63-linked ubiquitination of IRF7.TARBP2 通过抑制 TRAF6 介导的 IRF7 的 K63 链接泛素化来抑制 IRF7 的激活。
Mol Immunol. 2019 May;109:116-125. doi: 10.1016/j.molimm.2019.02.019. Epub 2019 Mar 27.
8
K63-linked ubiquitination in kinase activation and cancer.激酶激活和癌症中的 K63 链接泛素化。
Front Oncol. 2012 Jan 31;2:5. doi: 10.3389/fonc.2012.00005. eCollection 2012.
9
Trabid inhibits hepatocellular carcinoma growth and metastasis by cleaving RNF8-induced K63 ubiquitination of Twist1.Trabid 通过切割 RNF8 诱导的 Twist1 的 K63 泛素化来抑制肝癌生长和转移。
Cell Death Differ. 2019 Jan;26(2):306-320. doi: 10.1038/s41418-018-0119-2. Epub 2018 May 10.
10
Hepatitis B e Antigen Inhibits NF-κB Activity by Interrupting K63-Linked Ubiquitination of NEMO.乙型肝炎 e 抗原通过中断 NEMO 的 K63 链接泛素化来抑制 NF-κB 活性。
J Virol. 2019 Jan 4;93(2). doi: 10.1128/JVI.00667-18. Print 2019 Jan 15.

引用本文的文献

1
HDAC1/2-mediated deacetylation of KLF9 promotes the malignant progression of nasopharyngeal carcinoma via CDH17.HDAC1/2介导的KLF9去乙酰化通过CDH17促进鼻咽癌的恶性进展。
Oncogene. 2025 Jul 4. doi: 10.1038/s41388-025-03471-4.
2
Protein post-translational modifications in serine synthetic pathway: functions and molecular mechanisms.丝氨酸合成途径中的蛋白质翻译后修饰:功能与分子机制
Cell Commun Signal. 2025 Jul 1;23(1):311. doi: 10.1186/s12964-025-02327-4.
3
E3 ligase TRIM22 promotes melanoma proliferation by regulating cell cycle progression through K63-linked ubiquitination of p21.

本文引用的文献

1
RNF8-mediated regulation of Akt promotes lung cancer cell survival and resistance to DNA damage.RNF8 介导的 Akt 调节促进肺癌细胞存活和抵抗 DNA 损伤。
Cell Rep. 2021 Oct 19;37(3):109854. doi: 10.1016/j.celrep.2021.109854.
2
Loss of TRIM31 promotes breast cancer progression through regulating K48- and K63-linked ubiquitination of p53.TRIM31 的缺失通过调节 p53 的 K48-和 K63 连接泛素化来促进乳腺癌的进展。
Cell Death Dis. 2021 Oct 14;12(10):945. doi: 10.1038/s41419-021-04208-3.
3
Uev1A promotes breast cancer cell migration by up-regulating CT45A expression via the AKT pathway.
E3 连接酶TRIM22通过对p21进行K63连接的泛素化修饰来调控细胞周期进程,从而促进黑色素瘤的增殖。
Sci Rep. 2025 Jul 1;15(1):22311. doi: 10.1038/s41598-025-06348-4.
4
EBBP-Mediated Integrated Stress Response Attenuates Anthracycline-Induced Cardiotoxicity by Inhibiting the Ferroptosis of Cardiomyocytes.EBBP介导的综合应激反应通过抑制心肌细胞铁死亡减轻蒽环类药物诱导的心脏毒性。
Adv Sci (Weinh). 2025 Jun 10:e02726. doi: 10.1002/advs.202502726.
5
GPX4 knockdown suppresses M2 macrophage polarization in gastric cancer by modulating kynurenine metabolism.GPX4基因敲低通过调节犬尿氨酸代谢抑制胃癌中M2巨噬细胞极化。
Theranostics. 2025 Apr 22;15(12):5826-5845. doi: 10.7150/thno.108817. eCollection 2025.
6
Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.丝切蛋白与线粒体:肌动蛋白动力学之外的功能
Int J Mol Sci. 2025 Apr 25;26(9):4094. doi: 10.3390/ijms26094094.
7
The E3 Ubiquitin Ligase ARIH1 Facilitates Colorectal Cancer Progression by Promoting Oxidative Phosphorylation via the Mitochondrial Translocation of K63-Linked Ubiquitinated PHB1.E3泛素连接酶ARIH1通过促进K63连接的泛素化PHB1的线粒体易位来推动氧化磷酸化,从而促进结直肠癌进展。
Adv Sci (Weinh). 2025 Apr 26:e2501017. doi: 10.1002/advs.202501017.
8
Localized K63 Ubiquitin Signaling Is Regulated by VCP/p97 During Oxidative Stress.在氧化应激期间,局部K63泛素信号由VCP/p97调控。
Mol Cell Proteomics. 2025 Mar;24(3):100920. doi: 10.1016/j.mcpro.2025.100920. Epub 2025 Jan 28.
9
TRIM25: A Global Player of Cell Death Pathways and Promising Target of Tumor-Sensitizing Therapies.TRIM25:细胞死亡途径的全球参与者及肿瘤增敏治疗的潜在靶点
Cells. 2025 Jan 7;14(2):65. doi: 10.3390/cells14020065.
10
DCAF13-mediated K63-linked ubiquitination of RNA polymerase I promotes uncontrolled proliferation in Breast Cancer.DCAF13介导的RNA聚合酶I的K63连接泛素化促进乳腺癌的失控增殖。
Nat Commun. 2025 Jan 9;16(1):557. doi: 10.1038/s41467-025-55851-9.
Uev1A 通过 AKT 通路上调 CT45A 表达促进乳腺癌细胞迁移。
BMC Cancer. 2021 Sep 9;21(1):1012. doi: 10.1186/s12885-021-08750-3.
4
TRIM15 and CYLD regulate ERK activation via lysine-63-linked polyubiquitination.TRIM15 和 CYLD 通过赖氨酸 63 连接的多泛素化调节 ERK 激活。
Nat Cell Biol. 2021 Sep;23(9):978-991. doi: 10.1038/s41556-021-00732-8. Epub 2021 Sep 8.
5
The deubiquitinase USP10 restores PTEN activity and inhibits non-small cell lung cancer cell proliferation.去泛素化酶 USP10 可恢复 PTEN 的活性并抑制非小细胞肺癌细胞的增殖。
J Biol Chem. 2021 Sep;297(3):101088. doi: 10.1016/j.jbc.2021.101088. Epub 2021 Aug 18.
6
Deubiquitinase PSMD14 promotes ovarian cancer progression by decreasing enzymatic activity of PKM2.去泛素化酶 PSMD14 通过降低 PKM2 的酶活性促进卵巢癌进展。
Mol Oncol. 2021 Dec;15(12):3639-3658. doi: 10.1002/1878-0261.13076. Epub 2021 Aug 25.
7
Understanding the DNA double-strand break repair and its therapeutic implications.了解DNA双链断裂修复及其治疗意义。
DNA Repair (Amst). 2021 Oct;106:103177. doi: 10.1016/j.dnarep.2021.103177. Epub 2021 Jul 9.
8
Targeted Drug Delivery: Trends and Perspectives.靶向药物递送:趋势与展望。
Curr Drug Deliv. 2021;18(10):1435-1455. doi: 10.2174/1567201818666210609161301.
9
K63-linked ubiquitination of DYRK1A by TRAF2 alleviates Sprouty 2-mediated degradation of EGFR.TRAF2 通过 K63 连接的泛素化作用缓解了 DYRK1A 对 EGFR 的 Sprouty2 介导的降解。
Cell Death Dis. 2021 Jun 11;12(6):608. doi: 10.1038/s41419-021-03887-2.
10
The Carcinogen Cadmium Activates Lysine 63 (K63)-Linked Ubiquitin-Dependent Signaling and Inhibits Selective Autophagy.致癌物镉激活赖氨酸63(K63)连接的泛素依赖性信号传导并抑制选择性自噬。
Cancers (Basel). 2021 May 20;13(10):2490. doi: 10.3390/cancers13102490.