Stabilization of ATF5 by TAK1–Nemo-Like Kinase Critically Regulates the Interleukin-1β-Stimulated C/EBP Signaling Pathway

Ze-Yan Zhang; Shang-Ze Li; Hui-Hui Zhang; Qu-Ran Wu; Jun Gong; Tong Liang

首页> 外文期刊>Molecular and Cellular Biology >Stabilization of ATF5 by TAK1–Nemo-Like Kinase Critically Regulates the Interleukin-1β-Stimulated C/EBP Signaling Pathway

【24h】

Stabilization of ATF5 by TAK1–Nemo-Like Kinase Critically Regulates the Interleukin-1β-Stimulated C/EBP Signaling Pathway

机译：TAK1-Nemo-like激酶稳定ATF5关键性调节白介素1β刺激的C / EBP信号通路。

获取原文

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

Interleukin-1β (IL-1β) is a key proinflammatory cytokine that initiates several signaling cascades, including those involving CCAAT/enhancer binding proteins (C/EBPs). The mechanism by which IL-1β propagates a signal that activates C/EBP has remained elusive. Nemo-like kinase (NLK) is a mitogen-activated protein kinase (MAPK)-like kinase associated with many pathways and phenotypes that are not yet well understood. Using a luciferase reporter screen, we found that IL-1β-induced C/EBP activation was positively regulated by NLK. Overexpression of NLK activated C/EBP and potentiated IL-1β-triggered C/EBP activation, whereas knockdown or knockout of NLK had the opposite effect. NLK interacted with activating transcription factor 5 (ATF5) and inhibited the proteasome-dependent degradation of ATF5 in a kinase-independent manner. Consistently, NLK deficiency resulted in decreased levels of ATF5. NLK cooperated with ATF5 to activate C/EBP, whereas NLK could not activate C/EBP upon knockdown of ATF5. Moreover, TAK1, a downstream effector of IL-1β that acts upstream of NLK, mimicked the ability of NLK to stabilize ATF5 and activate C/EBP. Thus, our findings reveal the TAK1-NLK pathway as a novel regulator of basal or IL-1β-triggered C/EBP activation though stabilization of ATF5.

机译：白介素-1β（IL-1β）是一种重要的促炎细胞因子，可引发多种信号级联反应，包括涉及CCAAT /增强子结合蛋白（C / EBPs）的级联反应。 IL-1β传播激活C / EBP的信号的机制仍然难以捉摸。 Nemo-like激酶（NLK）是一种与许多尚未充分了解的途径和表型相关的促分裂原活化蛋白激酶（MAPK）-样激酶。使用萤光素酶报道分子筛选，我们发现NLK正调控IL-1β诱导的C / EBP激活。 NLK的过表达激活C / EBP和IL-1β触发的C / EBP增强激活，而敲除或敲除NLK具有相反的作用。 NLK与活化转录因子5（ATF5）相互作用，并以激酶非依赖性方式抑制ATF5的蛋白酶体依赖性降解。一致地，NLK缺乏导致ATF5水平降低。 NLK与ATF5合作激活C / EBP，而NLK在ATF5敲低后无法激活C / EBP。此外，TAK1（IL-1β的下游效应物，在NLK的上游起作用）模仿了NLK稳定ATF5和激活C / EBP的能力。因此，我们的发现揭示了TAK1-NLK途径是通过ATF5稳定而作为基础或IL-1β触发的C / EBP激活的新型调节剂。

著录项

来源
《Molecular and Cellular Biology》 |2015年第5期|共11页
作者
Ze-Yan Zhang; Shang-Ze Li; Hui-Hui Zhang; Qu-Ran Wu; Jun Gong; Tong Liang;
展开▼
作者单位

展开▼
收录信息
原文格式 PDF
正文语种
中图分类细胞生物学;
关键词

相似文献

外文文献
中文文献
专利

1. Transforming Growth Factor β-activated Kinase 1 (TAK1) Kinase Adaptor, TAK1-binding Protein 2, Plays Dual Roles in TAK1 Signaling by Recruiting Both an Activator and an Inhibitor of TAK1 Kinase in Tumor Necrosis Factor Signaling Pathway [J] . Peter Broglie, Kunihiro Matsumoto, Shizuo Akira, The Journal of biological chemistry . 2010,第4期

机译：转化生长因子β-活化激酶1（TAK1）激酶适配器，TAK1结合蛋白2，通过在肿瘤坏死因子信号通路中募集AVER1激酶和TAK1激酶的抑制剂在TAK1信号传导中起双重作用
2. An IFN-γ-stimulated ATF6-C/EBP-SS-signaling pathway critical for the expression of Death Associated Protein Kinase 1 and induction of autophagy [J] . Padmaja Gade, Girish Ramachandran, Uday B. Maachani, Proceedings of the National Academy of Sciences of the United States of America . 2012,第26期

机译：IFN-γ刺激的ATF6-C / EBP-SS信号通路对于死亡相关蛋白激酶1的表达和自噬的诱导至关重要
3. Interleukin-1 (IL-1) Receptor-Associated Kinase Leads to Activation of TAK1 by Inducing TAB2 Translocation in the IL-1 Signaling Pathway [J] . Giichi Takaesu, Jun Ninomiya-Tsuji, Satoshi Kishida, Molecular and Cellular Biology . 2001,第7期

机译：白介素-1（IL-1）受体相关的激酶通过诱导IL-1信号通路中的TAB2易位导致TAK1激活。
4. Sustained Static Pressure Stimulates Proliferation of Cultured Smooth Muscle Cells Via the Extracellular Signal-Regulated Kinase Pathway [C] . D.X. Luo, C.L. Xia, S.Y. He, World Congress on Heart Disease . 2007

机译：持续的静压刺激通过细胞外信号调节激酶途径刺激培养的平滑肌细胞的增殖
5. Intracellular signaling pathways regulating hepatic apolipoprotein B100 production: Role of mitogen -activated protein kinases (MAPKs) and inhibitor of NFkappaB kinase (IKK)-NFkappaB. [D] . Tsai, Julie Wen-chia. 2009

机译：调节肝载脂蛋白B100产生的细胞内信号传导途径：促分裂原活化蛋白激酶（MAPK）和NFkappBB激酶（IKK）-NFkappaB抑制剂的作用。
6. Stabilization of ATF5 by TAK1–Nemo-Like Kinase Critically Regulates the Interleukin-1β-Stimulated C/EBP Signaling Pathway [O] . Ze-Yan Zhang, Shang-Ze Li, Hui-Hui Zhang, 2015

机译：TAK1-Nemo-like激酶稳定ATF5关键调节白介素1β刺激的C / EBP信号通路。
7. Transforming Growth Factor β-activated Kinase 1 (TAK1) Kinase Adaptor, TAK1-binding Protein 2, Plays Dual Roles in TAK1 Signaling by Recruiting Both an Activator and an Inhibitor of TAK1 Kinase in Tumor Necrosis Factor Signaling Pathway* [O] . Broglie, Peter, Matsumoto, Kunihiro, Akira, Shizuo, 2009

机译：转化生长因子β活化激酶1（TAK1）激酶适配器，TAK1结合蛋白2，通过在肿瘤坏死因子信号通路中募集TAK1激酶的激活剂和抑制剂，在TAK1信号中起双重作用*
8. Small Scale Proteomics Approach for Identifying Proteins Regulated by the Breast Tumor Kinase BRK Signal Transduction Pathway. [R] . Tyner, A. L. 2002

机译：用于鉴定由乳腺肿瘤激酶BRK信号转导途径调节的蛋白质的小规模蛋白质组学方法。

Stabilization of ATF5 by TAK1–Nemo-Like Kinase Critically Regulates the Interleukin-1β-Stimulated C/EBP Signaling Pathway

摘要

著录项

相似文献

相关主题

期刊订阅