• 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

靶向假激酶TRIB3为急性早幼粒细胞白血病带来了一种新的治疗选择。

Targeting pseudokinase TRIB3 brings about a new therapeutic option for acute promyelocytic leukemia.

作者信息

Li Ke, Wang Feng, Hu Zhuo-Wei

机构信息

Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Immunology and Cancer Pharmacology Group, State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

出版信息

Mol Cell Oncol. 2017 Jun 16;4(4):e1337547. doi: 10.1080/23723556.2017.1337547. eCollection 2017.

DOI:10.1080/23723556.2017.1337547
PMID:28868348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5540211/
Abstract

Pseudokinase tribbles (Trib) family, and , but not , act as oncogene to drive acute leukemia by destabilizing the myeloid transcription factor CCAAT/enhancer-binding protein α (C/EBPα) and inhibiting myeloid differentiation. A recent study identifies pseudokinase TRIB3 as an important factor in acute promyelocytic leukemia (APL) progression and therapy resistance. Targeting TRIB3 may provide a novel therapeutic approach for APL.

摘要

假激酶TRIBbles(Trib)家族中的TRIB1和TRIB2而非TRIB3,作为癌基因通过使髓系转录因子CCAAT/增强子结合蛋白α(C/EBPα)不稳定并抑制髓系分化来驱动急性白血病。最近一项研究确定假激酶TRIB3是急性早幼粒细胞白血病(APL)进展和治疗耐药的一个重要因素。靶向TRIB3可能为APL提供一种新的治疗方法。

相似文献

1
Targeting pseudokinase TRIB3 brings about a new therapeutic option for acute promyelocytic leukemia.靶向假激酶TRIB3为急性早幼粒细胞白血病带来了一种新的治疗选择。
Mol Cell Oncol. 2017 Jun 16;4(4):e1337547. doi: 10.1080/23723556.2017.1337547. eCollection 2017.
2
Differential ability of Tribbles family members to promote degradation of C/EBPalpha and induce acute myelogenous leukemia.Tribbles 家族成员促进 C/EBPalpha 降解和诱导急性髓系白血病的差异能力。
Blood. 2010 Aug 26;116(8):1321-8. doi: 10.1182/blood-2009-07-229450. Epub 2010 Apr 21.
3
TRIB3 Promotes APL Progression through Stabilization of the Oncoprotein PML-RARα and Inhibition of p53-Mediated Senescence.TRIB3 通过稳定癌蛋白 PML-RARα 和抑制 p53 介导的衰老促进 APL 进展。
Cancer Cell. 2017 May 8;31(5):697-710.e7. doi: 10.1016/j.ccell.2017.04.006.
4
Inverse and correlative relationships between TRIBBLES genes indicate non-redundant functions during normal and malignant hemopoiesis.TRIBBLES基因之间的反向和相关关系表明其在正常和恶性造血过程中具有非冗余功能。
Exp Hematol. 2018 Oct;66:63-78.e13. doi: 10.1016/j.exphem.2018.07.005. Epub 2018 Jul 20.
5
The Critical Role of TRIB2 in Cancer and Therapy Resistance.TRIB2在癌症及治疗抗性中的关键作用
Cancers (Basel). 2021 May 30;13(11):2701. doi: 10.3390/cancers13112701.
6
Co-operative leukemogenesis in acute myeloid leukemia and acute promyelocytic leukemia reveals C/EBPα as a common target of TRIB1 and PML/RARA.急性髓系白血病和急性早幼粒细胞白血病中的协同白血病发生揭示了C/EBPα是TRIB1和PML/RARA的共同靶点。
Haematologica. 2016 Oct;101(10):1228-1236. doi: 10.3324/haematol.2015.138503. Epub 2016 Jul 6.
7
Nanobodies identify an activated state of the TRIB2 pseudokinase.纳米抗体鉴定 TRIB2 伪激酶的激活状态。
Structure. 2022 Nov 3;30(11):1518-1529.e5. doi: 10.1016/j.str.2022.08.006. Epub 2022 Sep 14.
8
TRIB3 Stabilizes High TWIST1 Expression to Promote Rapid APL Progression and ATRA Resistance.TRIB3 通过稳定 TWIST1 高表达促进 APL 的快速进展和 ATRA 耐药。
Clin Cancer Res. 2019 Oct 15;25(20):6228-6242. doi: 10.1158/1078-0432.CCR-19-0510. Epub 2019 Jun 24.
9
The Tribble with APL: A New Road to Therapy.APL 伴巨核细胞白血病:新的治疗途径。
Cancer Cell. 2017 May 8;31(5):612-613. doi: 10.1016/j.ccell.2017.04.011.
10
Tribbles homolog 2 (Trib2) and HoxA9 cooperate to accelerate acute myelogenous leukemia.TRIB2同源物2(Trib2)与HoxA9协同作用以加速急性髓性白血病。
Blood Cells Mol Dis. 2008 Jan-Feb;40(1):119-21. doi: 10.1016/j.bcmd.2007.06.005. Epub 2007 Nov 7.

引用本文的文献

1
PML-RARα interaction with TRIB3 impedes PPARγ/RXR function and triggers dyslipidemia in acute promyelocytic leukemia.PML-RARα 与 TRIB3 的相互作用抑制了 PPARγ/RXR 的功能,并在急性早幼粒细胞白血病中引发了血脂异常。
Theranostics. 2020 Aug 15;10(22):10326-10340. doi: 10.7150/thno.45924. eCollection 2020.

本文引用的文献

1
TRIB3 Promotes APL Progression through Stabilization of the Oncoprotein PML-RARα and Inhibition of p53-Mediated Senescence.TRIB3 通过稳定癌蛋白 PML-RARα 和抑制 p53 介导的衰老促进 APL 进展。
Cancer Cell. 2017 May 8;31(5):697-710.e7. doi: 10.1016/j.ccell.2017.04.006.
2
TRB3 links insulin/IGF to tumour promotion by interacting with p62 and impeding autophagic/proteasomal degradations.TRB3 通过与 p62 相互作用并阻碍自噬/蛋白酶体降解,将胰岛素/胰岛素样生长因子与肿瘤促进联系起来。
Nat Commun. 2015 Aug 13;6:7951. doi: 10.1038/ncomms8951.
3
Resistance to therapy in acute promyelocytic leukemia.急性早幼粒细胞白血病的治疗耐药性。
N Engl J Med. 2014 Sep 18;371(12):1170-2. doi: 10.1056/NEJMc1409040.
4
Tribbles in acute leukemia.急性白血病中的类垂星体。
Blood. 2013 May 23;121(21):4265-70. doi: 10.1182/blood-2012-12-471300. Epub 2013 Apr 2.
5
Inhibition of α-helix-mediated protein-protein interactions using designed molecules.利用设计分子抑制α-螺旋介导的蛋白质-蛋白质相互作用。
Nat Chem. 2013 Mar;5(3):161-73. doi: 10.1038/nchem.1568.
6
TRB3 interacts with SMAD3 promoting tumor cell migration and invasion.TRB3 与 SMAD3 相互作用,促进肿瘤细胞迁移和侵袭。
J Cell Sci. 2011 Oct 1;124(Pt 19):3235-46. doi: 10.1242/jcs.082875. Epub 2011 Sep 6.
7
Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia.急性早幼粒细胞白血病中 MYC 染色体的复发性三体性源于 MYC 的增益。
J Exp Med. 2010 Nov 22;207(12):2581-94. doi: 10.1084/jem.20091071. Epub 2010 Nov 8.
8
Autophagy contributes to therapy-induced degradation of the PML/RARA oncoprotein.自噬有助于治疗诱导的 PML/RARA 癌蛋白降解。
Blood. 2010 Sep 30;116(13):2324-31. doi: 10.1182/blood-2010-01-261040. Epub 2010 Jun 23.
9
A sumoylation site in PML/RARA is essential for leukemic transformation.早幼粒细胞白血病/维甲酸受体α(PML/RARA)中的一个类泛素化位点对白血病转化至关重要。
Cancer Cell. 2005 Feb;7(2):143-53. doi: 10.1016/j.ccr.2005.01.005.
10
A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657.具有FLT3突变的急性早幼粒细胞白血病模型对维甲酸和一种受体酪氨酸激酶抑制剂SU11657有反应。
Blood. 2003 Apr 15;101(8):3188-97. doi: 10.1182/blood-2002-06-1800. Epub 2002 Dec 19.