个人中心| | 帮助
高级检索
当前位置： 首页 > 详情页

A mutation of cysteine 46 in IKK-β promotes mPGES-1 and caveolin-1 expression to exacerbate osteoclast differentiation and osteolysis.

| 认领 | 导出 | |

文献详情

资源类型：
WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
Zou Binhua[1,2] * ; Zhang Yueyang[1,2,3] * ; Li Ting[4] * ; Liu Juan[4] ; Deng Wende[1,2] ; Tan Yanhui[1,2] ; Yang Qin[1,2] ; Ding Zongbao[1,2] ; Liao Kangsheng[4] ; Xu Jialan[1,2] ; Pan Hudan[4] ; Li Xiaojuan[1,2,*1] ; Liu Liang[4,*2] ;
机构： [1]Laboratory of Anti-inflammatory and Immunomodulatory Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [2]Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [3]Clinical Pharmacology, The Third Affiliated Hospital of Sun-Yat-Sen University, Guangzhou 510630, China [4]State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China
出处：
DOI： 10.1016/j.bcp.2019.113762
ISSN：

关键词： IKK-β Osteoclast NFATc1 mPGES-1 Caveolin-1

摘要：
IKK-β is indispensable for inflammatory osteolysis, the functional residues of IKK-β are therapeutic drug targets for developing inhibitors to treat multiple diseases now. Thus it remains appealing to find the new residues of IKK-β to influence osteoclasts for alleviating bone loss diseases such as rheumatoid arthritis (RA). By employing IKK-β cysteine 46-A transgenic (IKK-βC46A) mice, we found that mutation of cysteine 46 to alanine in IKK-β exacerbated inflammatory bone destruction in vivo, and increased osteoclast differentiation and bone resorption ex vivo and in vitro. Consistent with these, IKK-β kinase activity as well as c-Fos, NFATc1 were up-regulated in bone marrow macrophages (BMMs) from IKK-βC46A mice during RANKL-induced osteoclastogenesis. Of interesting, we further identified and demonstrated that the expressions of mPGES-1 and caveolin-1 were heightened in BMMs of IKK-βC46A mice compared to those in WT mice in RANKL-induced osteoclastogenesis. Together, it revealed that mutating cysteine 46 in IKK-β could increase caveolin-1 and mPGES-1 expression to facilitate osteoclast differentiation and osteolysis. Cysteine 46 can serve as a novel target in IKK-β for designing inhibitors to treat osteolysis. Copyright © 2019 Elsevier Inc. All rights reserved.

基金：
National Natural Science Foundation of China (81773740, 81073119, and 81611130078), Guangzhou Science and Technology Plan Project (201804010027), the Natural Science Foundation of Guangdong Province (2015A030313287, 2018B030312010).
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2019]版：
大类 | 2 区 医学
小类 | 2 区 药学
最新[2025]版：
大类 | 2 区 医学
小类 | 2 区 药学
JCR分区：
出版当年[2018]版：
Q1 PHARMACOLOGY & PHARMACY
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY

影响因子： 最新[2023版] 最新五年平均 出版当年[2018版] 出版当年五年平均 出版前一年[2017版] 出版后一年[2019版]

第一作者：
第一作者机构： [1]Laboratory of Anti-inflammatory and Immunomodulatory Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [2]Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China
共同第一作者：
通讯作者：
通讯机构： [1]Laboratory of Anti-inflammatory and Immunomodulatory Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [2]Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [4]State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China [*1]Laboratory of Anti-inflammatory and Immunomodulatory Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China [*2]State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China
推荐引用方式(GB/T 7714)：
Zou Binhua,Zhang Yueyang,Li Ting,et al.A mutation of cysteine 46 in IKK-β promotes mPGES-1 and caveolin-1 expression to exacerbate osteoclast differentiation and osteolysis.[J].BIOCHEMICAL PHARMACOLOGY.2020,172:doi:10.1016/j.bcp.2019.113762.
APA：
Zou Binhua,Zhang Yueyang,Li Ting,Liu Juan,Deng Wende...&Liu Liang.(2020).A mutation of cysteine 46 in IKK-β promotes mPGES-1 and caveolin-1 expression to exacerbate osteoclast differentiation and osteolysis..BIOCHEMICAL PHARMACOLOGY,172,
MLA：
Zou Binhua,et al."A mutation of cysteine 46 in IKK-β promotes mPGES-1 and caveolin-1 expression to exacerbate osteoclast differentiation and osteolysis.".BIOCHEMICAL PHARMACOLOGY 172.(2020)

相关文献

[1]Eriodictyol Inhibits RANKL-Induced Osteoclast Formation and Function Via Inhibition of NFATc1 Activity. [2]Dendrobine attenuates osteoclast differentiation through modulating ROS/NFATc1/MMP9 pathway and prevents inflammatory bone destruction [3]Inhibitory Effects of Rhaponticin on Osteoclast Formation and Resorption by Targeting RANKL-Induced NFATc1 and ROS Activity [4]Inhibitory effects of Rhaponticin on osteoclast formation and resorption by targeting RANKL-induced NFATc1 and ROS activity (vol 12, 645140, 2021) [5]Cycloastragenol Attenuates Osteoclastogenesis and Bone Loss by Targeting RANKL-Induced Nrf2/Keap1/ARE, NF-κB, Calcium, and NFATc1 Pathways. [6]Sinomenine increases the methylation level at specific GCG site in mPGES-1 promoter to facilitate its specific inhibitory effect on mPGES-1. [7]Aconine inhibits RANKL-induced osteoclast differentiation in RAW2647 cells by suppressing NF-κB and NFATc1 activation and DC-STAMP expression [8]Dendrobine attenuates osteoclast differentiation through modulating ROS/NFATc1/ MMP9 pathway and prevents inflammatory bone destruction. [9]A novel RANKL-targeted flavonoid glycoside prevents osteoporosis through inhibiting NFATc1 and reactive oxygen species. [10]降糖补肾方对糖尿病大鼠IKKβ mRNA表达的影响

资源点击量：2020 今日访问量：0 总访问量：646 更新日期：2024-07-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 广东省中医院 技术支持：重庆聚合科技有限公司 地址：广州市越秀区大德路111号