检索结果-南通市图书馆

Inhibition of CD82 improves colitis by increasing NLRP3 deubiquitination by BRCC3

Cellular & Molecular Immunology 2023年第2期20卷 189-200页

作者： Jae-Sung Kim Hyo Keun Kim Joongho Lee Sein Jang euni cho Seok-Jun Mun Seokhyun Yoon Chul-Su Yang Department of Bionano Technology Hanyang UniversitySeoul04673Korea Institute of Natural Science&Technology Hanyang UniversityAnsan15588Korea Department of Molecular and Life Science Hanyang UniversityAnsan15588Korea Center for Bionano Intelligence Education and Research Ansan15588Korea Department of Computer Science College of SW ConvergenceDankook UniversityYongin16890Korea Department of Electronics&Electrical Engineering College of EngineeringDankook UniversityYongin16890Korea

CD82 is a transmembrane protein that is involved in cancer suppression and activates immune cells;however, information on the NLRP3 inflammasome is limited. Herein, we show that although CD82 suppressed the activation of the NLRP3 inflammasome in vivo and in vitro, CD82 deficiency decreased the severity of colitis in mice. Furthermore, two binding partners of CD82, NLRP3 and BRCC3, were identified. CD82 binding to these partners increased the degradation of NLRP3 by blocking BRCC3-dependent K63-specific deubiquitination. Previous studies have shown that CD82-specific bacteria in the colon microbiota called Bacteroides vulgatus (B. vulgatus) regulated the expression of CD82 and promoted the activation of the NLRP3 inflammasome. Accordingly, we observed that B. vulgatus administration increased mouse survival by mediating CD82 expression and activating NLRP3 in mice with colitis. Overall, this study showed that CD82 suppression reduced the pathogenesis of colitis by elevating the activation of the NLRP3 inflammasome through BRCC3-dependent K63 deubiquitination. Based on our findings, we propose that B. vulgatus is a novel therapeutic candidate for colitis.

关键词： CD82 NLRP3 BRCC3 Colitis Inflammation

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Dual alarmin-receptor-specific targeting peptide systems for treatment of sepsis

引用

Acta Pharmaceutica Sinica B 2024年第12期14卷 5451-5463页

作者： Mun, Seok-Jun cho, euni Gil, Woo Jin Kim, Seong Jae Kim, Hyo Keun Ham, Yu Seong Yang, Chul-Su Department of Bionano Engineering Hanyang University Seoul 04673 South Korea Center for Bionano Intelligence Education and Research Ansan 15588 South Korea Department of Molecular and Life Science Hanyang University Ansan 15588 South Korea Department of Medicinal and Life Science Hanyang University Ansan 15588 South Korea

The pathophysiology of sepsis is characterized by a systemic inflammatory response to infection;however, the cytokine blockade that targets a specific early inflammatory mediator, such as tumor necrosis factor, has shown disappointing results in clinical trials. During sepsis, excessive endotoxins are internalized into the cytoplasm of immune cells, resulting in dysregulated pyroptotic cell death, which induces the leakage of late mediator alarmins such as HMGB1 and PTX3. As late mediators of lethal sepsis, overwhelming amounts of alarmins bind to high-affinity TLR4/MD2 and low-affinity RAGE receptors, thereby amplifying inflammation during early-stage sepsis. In this study, we developed a novel alarmin/receptor-targeting system using a TLR4/MD2/RAGE-blocking peptide (TMR peptide) derived from the HMGB1/PTX3-receptors interacting motifs. The TMR peptide successfully attenuated HMGB1/PTX3- and LPS-mediated inflammatory cytokine production by impairing its interactions with TLR4 and RAGE. Moreover, we developed TMR peptide-conjugated liposomes (TMR-Lipo) to improve the peptide pharmacokinetics. In combination therapy, moderately antibiotic-loaded TMR-Lipo demonstrated a significant therapeutic effect in a mouse model of cecal ligation- and puncture-induced sepsis. The identification of these peptides will pave the way for the development of novel pharmacological tools for sepsis therapy. © 2024 The Authors

关键词： Antibiotics High mobility group box 1 Liposome Pentraxin 3 Sepsis

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：