• 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

相似文献

1
Targeted deletion of hepatocyte Ikkbeta confers growth advantages.肝细胞Ikkβ的靶向缺失赋予生长优势。
Biochem Biophys Res Commun. 2009 Mar 6;380(2):349-54. doi: 10.1016/j.bbrc.2009.01.085. Epub 2009 Jan 24.
2
Loss of hepatic NF-kappa B activity enhances chemical hepatocarcinogenesis through sustained c-Jun N-terminal kinase 1 activation.肝脏核因子-κB活性丧失通过持续激活c-Jun氨基末端激酶1增强化学性肝癌发生。
Proc Natl Acad Sci U S A. 2006 Jul 11;103(28):10544-51. doi: 10.1073/pnas.0603499103. Epub 2006 Jun 28.
3
IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis.IKKβ 将肝细胞死亡与细胞因子驱动的代偿性增殖联系起来，这种增殖促进化学性肝癌发生。
Cell. 2005 Jul 1;121(7):977-90. doi: 10.1016/j.cell.2005.04.014.
4
Hepatocyte-specific inhibitor-of-kappaB-kinase deletion triggers the innate immune response and promotes earlier cell proliferation during liver regeneration.肝细胞特异性κB激酶抑制因子缺失引发先天性免疫反应并促进肝再生过程中更早的细胞增殖。
Hepatology. 2008 Jun;47(6):2036-50. doi: 10.1002/hep.22264.
5
Neuron-derived orphan receptor 1 promotes proliferation of quiescent hepatocytes.神经元衍生孤儿受体 1 促进静止肝细胞的增殖。
Gastroenterology. 2013 Jun;144(7):1518-1529.e3. doi: 10.1053/j.gastro.2013.02.027. Epub 2013 Feb 24.
6
High expression levels of IKKalpha and IKKbeta are necessary for the malignant properties of liver cancer.IKKα 和 IKKβ 的高表达水平对于肝癌的恶性特性是必要的。
Int J Cancer. 2010 Mar 1;126(5):1263-74. doi: 10.1002/ijc.24854.
7
The transforming growth factor-α and cyclin D1 genes are direct targets of β-catenin signaling in hepatocyte proliferation.β-连环蛋白信号通路在肝实质细胞增殖中可直接靶向转化生长因子-α和细胞周期蛋白 D1 基因。
J Hepatol. 2011 Jul;55(1):86-95. doi: 10.1016/j.jhep.2010.10.021. Epub 2010 Nov 30.
8
Inhibitory role of Smad7 in hepatocarcinogenesis in mice and in vitro.Smad7 在小鼠和体外肝癌发生中的抑制作用。
J Pathol. 2013 Aug;230(4):441-52. doi: 10.1002/path.4206.
9
Hepatocyte IKKbeta/NF-kappaB inhibits tumor promotion and progression by preventing oxidative stress-driven STAT3 activation.肝细胞 IKKβ/NF-κB 通过阻止氧化应激驱动的 STAT3 激活来抑制肿瘤促进和进展。
Cancer Cell. 2010 Mar 16;17(3):286-97. doi: 10.1016/j.ccr.2009.12.048.
10
Cyclin D1 induction through IkappaB kinase beta/nuclear factor-kappaB pathway is responsible for arsenite-induced increased cell cycle G1-S phase transition in human keratinocytes.通过IκB激酶β/核因子-κB途径诱导细胞周期蛋白D1，导致亚砷酸盐诱导人角质形成细胞的细胞周期G1-S期转换增加。
Cancer Res. 2005 Oct 15;65(20):9287-93. doi: 10.1158/0008-5472.CAN-05-0469.

引用本文的文献

1
A Modified Protocol of Diethylnitrosamine Administration in Mice to Model Hepatocellular Carcinoma.一种改良的二乙基亚硝胺在小鼠体内诱导肝癌模型的方案。
Int J Mol Sci. 2020 Jul 30;21(15):5461. doi: 10.3390/ijms21155461.
2
An IKK/NF-κB Activation/p53 Deletion Sequence Drives Liver Carcinogenesis and Tumor Differentiation.IKK/NF-κB激活/p53缺失序列驱动肝癌发生和肿瘤分化。
Cancers (Basel). 2019 Sep 21;11(10):1410. doi: 10.3390/cancers11101410.
3
New insights in hepatocellular carcinoma: from bench to bedside.肝细胞癌的新见解：从基础到临床。
Ann Transl Med. 2013 Jul;1(2):15. doi: 10.3978/j.issn.2305-5839.2013.01.06.
4
Hypothesis: Targeted deletion upregulates MIF signaling responsiveness and MHC class II expression in mouse hepatocytes.假设：靶向缺失可上调小鼠肝细胞中巨噬细胞移动抑制因子（MIF）信号反应性及主要组织相容性复合体II类分子（MHC class II）的表达。
Hepat Med. 2010 Mar;2010(2):39-47. doi: 10.2147/HMER.S7208.
5
The NF-κB subunit RelA/p65 is dispensable for successful liver regeneration after partial hepatectomy in mice.NF-κB 亚基 RelA/p65 在小鼠肝部分切除术后的肝再生中不是必需的。
PLoS One. 2012;7(10):e46469. doi: 10.1371/journal.pone.0046469. Epub 2012 Oct 1.
6
IκB kinase β regulates epithelium migration during corneal wound healing.IKKβ 调控角膜伤口愈合过程中的上皮细胞迁移。
PLoS One. 2011 Jan 17;6(1):e16132. doi: 10.1371/journal.pone.0016132.
7
NF-κB, JNK, and TLR Signaling Pathways in Hepatocarcinogenesis.NF-κB、JNK 和 TLR 信号通路在肝癌发生中的作用。
Gastroenterol Res Pract. 2010;2010:367694. doi: 10.1155/2010/367694. Epub 2010 Nov 28.
8
Ectopic expression of CD74 in Ikkβ-deleted mouse hepatocytes.Ikkβ 缺失的鼠肝细胞中 CD74 的异位表达。
Acta Histochem. 2011 Jul;113(4):428-35. doi: 10.1016/j.acthis.2010.03.004. Epub 2010 Jun 1.
9
Hepatocyte IKKbeta/NF-kappaB inhibits tumor promotion and progression by preventing oxidative stress-driven STAT3 activation.肝细胞 IKKβ/NF-κB 通过阻止氧化应激驱动的 STAT3 激活来抑制肿瘤促进和进展。
Cancer Cell. 2010 Mar 16;17(3):286-97. doi: 10.1016/j.ccr.2009.12.048.
10
Mechanisms of liver disease: cross-talk between the NF-kappaB and JNK pathways.肝脏疾病的发病机制：NF-κB 和 JNK 通路的串扰。
Biol Chem. 2009 Oct;390(10):965-76. doi: 10.1515/BC.2009.111.

本文引用的文献

1
Hepatocyte necrosis induced by oxidative stress and IL-1 alpha release mediate carcinogen-induced compensatory proliferation and liver tumorigenesis.氧化应激诱导的肝细胞坏死和白细胞介素-1α释放介导致癌物诱导的代偿性增殖和肝脏肿瘤发生。
Cancer Cell. 2008 Aug 12;14(2):156-65. doi: 10.1016/j.ccr.2008.06.016.
2
IKK1 and IKK2 cooperate to maintain bile duct integrity in the liver.IKK1和IKK2协同作用以维持肝脏中胆管的完整性。
Proc Natl Acad Sci U S A. 2008 Jul 15;105(28):9733-8. doi: 10.1073/pnas.0800198105. Epub 2008 Jul 7.
3
Fate-mapping evidence that hepatic stellate cells are epithelial progenitors in adult mouse livers.命运图谱证据表明肝星状细胞是成年小鼠肝脏中的上皮祖细胞。
Stem Cells. 2008 Aug;26(8):2104-13. doi: 10.1634/stemcells.2008-0115. Epub 2008 May 29.
4
Hepatocyte-specific inhibitor-of-kappaB-kinase deletion triggers the innate immune response and promotes earlier cell proliferation during liver regeneration.肝细胞特异性κB激酶抑制因子缺失引发先天性免疫反应并促进肝再生过程中更早的细胞增殖。
Hepatology. 2008 Jun;47(6):2036-50. doi: 10.1002/hep.22264.
5
Tumor suppressor and hepatocellular carcinoma.肿瘤抑制与肝细胞癌
World J Gastroenterol. 2008 Mar 21;14(11):1720-33. doi: 10.3748/wjg.14.1720.
6
A role for IkappaB kinase 2 in bipolar spindle assembly.IκB激酶2在双极纺锤体组装中的作用。
Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):16940-5. doi: 10.1073/pnas.0706493104. Epub 2007 Oct 15.
7
Gender disparity in liver cancer due to sex differences in MyD88-dependent IL-6 production.由于依赖MyD88的白细胞介素-6产生存在性别差异，导致肝癌中的性别差异。
Science. 2007 Jul 6;317(5834):121-4. doi: 10.1126/science.1140485.
8
Loss of Ikkbeta promotes migration and proliferation of mouse embryo fibroblast cells.Ikkbeta缺失促进小鼠胚胎成纤维细胞的迁移和增殖。
J Biol Chem. 2006 Dec 1;281(48):37142-9. doi: 10.1074/jbc.M603631200. Epub 2006 Sep 11.
9
Immune-privileged embryonic Swiss mouse STO and STO cell-derived progenitor cells: major histocompatibility complex and cell differentiation antigen expression patterns resemble those of human embryonic stem cell lines.免疫特惠的胚胎瑞士小鼠STO及STO细胞衍生的祖细胞：主要组织相容性复合体和细胞分化抗原表达模式类似于人类胚胎干细胞系。
Immunology. 2006 Sep;119(1):98-115. doi: 10.1111/j.1365-2567.2006.02412.x. Epub 2006 Jul 10.
10
Disrupted NF- kappa B activation after partial hepatectomy does not impair hepatocyte proliferation in rats.大鼠部分肝切除术后NF-κB激活受干扰并不损害肝细胞增殖。
World J Gastroenterol. 2005 Dec 14;11(46):7345-50. doi: 10.3748/wjg.v11.i46.7345.

肝细胞Ikkβ的靶向缺失赋予生长优势。

Targeted deletion of hepatocyte Ikkbeta confers growth advantages.

作者信息

Koch Katherine S, Maeda Shin, He Guobin, Karin Michael, Leffert Hyam L

机构信息

Hepatocyte Growth Control and Stem Cell Laboratory, School of Medicine, University of California at San Diego, 9500 Gilman Drive MC 0636, La Jolla, CA 92093-0636, USA.

出版信息

Biochem Biophys Res Commun. 2009 Mar 6;380(2):349-54. doi: 10.1016/j.bbrc.2009.01.085. Epub 2009 Jan 24.

DOI:10.1016/j.bbrc.2009.01.085
PMID:19171122
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2663043/
Abstract

Mice lacking hepatocyte IKKbeta (Ikkbeta(Delta hep)) are defective in TNFalpha-activation of hepatocellular transcription factor NF-kappaB, and highly susceptible to hepatotoxicity. Following diethylnitrosamine (DEN) exposure, Ikkbeta(Delta hep) mice develop more hepatocellular carcinoma (HCC) than control mice due partly to enhanced DEN-induced hepatocyte death. Here we show that Ikkbeta(Delta hep) hepatocytes display growth advantages over normal hepatocytes consisting of precocious PCNA and cyclin D1 expression during liver regeneration (shortened hepatocyte G(0)-->G(1) transitions), and enhanced recovery efficiency, cyclin D1 expression and cell proliferation after plating. Ex vivo deletion of Ikkbeta also accelerates hepatocyte growth. Ikkbeta(Delta hep) hepatocyte proliferative responses show heightened sensitivity to TGFalpha and TNFalpha, and heightened expression of fibronectin, collagens I/III, nidogen, beta-actin and integrin beta1 mRNAs. These findings suggest that altered mitogen signaling and expression of extracellular matrix and its associated components underlie growth advantages. Increased HCC development in Ikkbeta(Delta hep) mice may also be caused by growth advantages of surviving Ikkbeta-deleted hepatocytes.

摘要

缺乏肝细胞IKKβ（Ikkbeta(Delta hep)）的小鼠在肿瘤坏死因子α激活肝细胞转录因子NF-κB方面存在缺陷，并且对肝毒性高度敏感。在接触二乙基亚硝胺（DEN）后，Ikkbeta(Delta hep)小鼠比对照小鼠发生更多的肝细胞癌（HCC），部分原因是DEN诱导的肝细胞死亡增加。在此我们表明，Ikkbeta(Delta hep)肝细胞在肝再生过程中（肝细胞G(0)到G(1)转换缩短），通过过早表达增殖细胞核抗原（PCNA）和细胞周期蛋白D1，显示出相对于正常肝细胞的生长优势，并且在接种后恢复效率、细胞周期蛋白D1表达和细胞增殖增强。体外缺失IKKβ也会加速肝细胞生长。Ikkbeta(Delta hep)肝细胞增殖反应对转化生长因子α（TGFα）和肿瘤坏死因子α显示出更高的敏感性，并且纤连蛋白、I/III型胶原、巢蛋白、β-肌动蛋白和整合素β1 mRNA的表达增加。这些发现表明，有丝分裂原信号改变以及细胞外基质及其相关成分的表达是生长优势的基础。Ikkbeta(Delta hep)小鼠中HCC发生增加也可能是由于存活的IKKβ缺失肝细胞的生长优势所致。