• 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

更正:阿克拉霉素A通过p38丝裂原活化蛋白激酶介导的红系分化使K562慢性髓系白血病细胞对伊马替尼敏感。

Correction: Aclacinomycin A Sensitizes K562 Chronic Myeloid Leukemia Cells to Imatinib through p38MAPK-Mediated Erythroid Differentiation.

作者信息

Lee Yueh-Lun, Chen Chih-Wei, Liu Fu-Hwa, Huang Yu-Wen, Huang Huei-Mei

出版信息

PLoS One. 2017 Oct 11;12(10):e0186528. doi: 10.1371/journal.pone.0186528. eCollection 2017.

DOI:10.1371/journal.pone.0186528
PMID:29020096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5636156/
Abstract

[This corrects the article DOI: 10.1371/journal.pone.0061939.].

摘要

[本文更正了文章的数字对象标识符:10.1371/journal.pone.0061939。]

相似文献

1
Correction: Aclacinomycin A Sensitizes K562 Chronic Myeloid Leukemia Cells to Imatinib through p38MAPK-Mediated Erythroid Differentiation.更正:阿克拉霉素A通过p38丝裂原活化蛋白激酶介导的红系分化使K562慢性髓系白血病细胞对伊马替尼敏感。
PLoS One. 2017 Oct 11;12(10):e0186528. doi: 10.1371/journal.pone.0186528. eCollection 2017.
2
Correction: MPT0B169, a New Antitubulin Agent, Inhibits Bcr-Abl Expression and Induces Mitochondrion-Mediated Apoptosis in Nonresistant and Imatinib-Resistant Chronic Myeloid Leukemia Cells.更正:新型抗微管蛋白剂MPT0B169抑制非耐药和伊马替尼耐药的慢性髓性白血病细胞中的Bcr-Abl表达并诱导线粒体介导的凋亡。
PLoS One. 2017 Oct 11;12(10):e0186531. doi: 10.1371/journal.pone.0186531. eCollection 2017.
3
Correction: MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.更正:微小RNA-1301介导的RanGAP1下调诱导BCR-ABL核内滞留以增强伊马替尼对慢性粒细胞白血病细胞的疗效。
PLoS One. 2017 Mar 7;12(3):e0173828. doi: 10.1371/journal.pone.0173828. eCollection 2017.
4
Spred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cells.Spred2调节伊马替尼诱导的慢性粒细胞白血病细胞的红系分化。
PLoS One. 2015 Feb 17;10(2):e0117573. doi: 10.1371/journal.pone.0117573. eCollection 2015.
5
Correction: GATA2 Inhibition Sensitizes Acute Myeloid Leukemia Cells to Chemotherapy.更正:GATA2抑制使急性髓系白血病细胞对化疗敏感。
PLoS One. 2017 Mar 28;12(3):e0175005. doi: 10.1371/journal.pone.0175005. eCollection 2017.
6
MYC antagonizes the differentiation induced by imatinib in chronic myeloid leukemia cells through downregulation of p27(KIP1.).MYC 通过下调 p27(KIP1.)拮抗伊马替尼诱导的慢性髓系白血病细胞分化。
Oncogene. 2013 Apr 25;32(17):2239-46. doi: 10.1038/onc.2012.246. Epub 2012 Jun 18.
7
Enforced expression of Bcl-XS induces differentiation and sensitizes chronic myelogenous leukemia-blast crisis K562 cells to 1-beta-D-arabinofuranosylcytosine-mediated differentiation and apoptosis.Bcl-XS的强制表达诱导分化,并使慢性粒细胞白血病急变期K562细胞对1-β-D-阿拉伯呋喃糖基胞嘧啶介导的分化和凋亡敏感。
Cell Growth Differ. 1996 Dec;7(12):1617-23.
8
Knock-down of CIAPIN1 sensitizes K562 chronic myeloid leukemia cells to Imatinib by regulation of cell cycle and apoptosis-associated members via NF-κB and ERK5 signaling pathway.敲低 CIAPIN1 通过调控 NF-κB 和 ERK5 信号通路,调节细胞周期和凋亡相关蛋白,使 K562 慢性髓系白血病细胞对伊马替尼敏感。
Biochem Pharmacol. 2016 Jan 1;99:132-45. doi: 10.1016/j.bcp.2015.12.002. Epub 2015 Dec 8.
9
Fast apoptosis and erythroid differentiation induced by imatinib mesylate in JURL-MK1 cells.甲磺酸伊马替尼诱导JURL-MK1细胞快速凋亡和红系分化。
J Cell Biochem. 2005 May 15;95(2):268-80. doi: 10.1002/jcb.20407.
10
Apoptosis and erythroid differentiation triggered by Bcr-Abl inhibitors in CML cell lines are fully distinguishable processes that exhibit different sensitivity to caspase inhibition.Bcr-Abl抑制剂在慢性粒细胞白血病细胞系中引发的凋亡和红系分化是完全可区分的过程,它们对胱天蛋白酶抑制表现出不同的敏感性。
Oncogene. 2007 Apr 12;26(17):2445-58. doi: 10.1038/sj.onc.1210034. Epub 2006 Oct 9.

本文引用的文献

1
Aclacinomycin A sensitizes K562 chronic myeloid leukemia cells to imatinib through p38MAPK-mediated erythroid differentiation.阿克拉霉素 A 通过 p38MAPK 介导的红系分化使 K562 慢性髓系白血病细胞对伊马替尼敏感。
PLoS One. 2013 Apr 17;8(4):e61939. doi: 10.1371/journal.pone.0061939. Print 2013.