科研成果详情

题名YOD1 sustains NOD2-mediated protective signaling in colitis by stabilizing RIPK2
作者
发表日期2024-09-27
发表期刊EMBO reports   影响因子和分区
语种英语
原始文献类型Journal Article
关键词Inflammatory Bowel Disease NOD2 RIPK2 Ubiquitination YOD1
其他关键词NF-KAPPA-B ; NOD2 ; BINDING ; A20 ; SUSCEPTIBILITY ; ENZYME
摘要Inflammatory bowel disease (IBD) is a disorder causing chronic inflammation in the gastrointestinal tract, and its pathophysiological mechanisms are still under investigation. Here, we find that mice deficient of YOD1, a deubiquitinating enzyme, are highly susceptible to dextran sulfate sodium (DSS)-induced colitis. The bone marrow transplantation experiment reveals that YOD1 derived from hematopoietic cells inhibits DSS colitis. Moreover, YOD1 exerts its protective role by promoting nucleotide-binding oligomerization domain 2 (NOD2)-mediated physiological inflammation in macrophages. Mechanistically, YOD1 inhibits the proteasomal degradation of receptor-interacting serine/threonine kinase 2 (RIPK2) by reducing its K48 polyubiquitination, thereby increasing RIPK2 abundance to enhance NOD2 signaling. Consistently, the protective function of muramyldipeptide, a NOD2 ligand, in experimental colitis is abolished in mice deficient of YOD1. Importantly, YOD1 is upregulated in colon-infiltrating macrophages in patients with colitis. Collectively, this study identifies YOD1 as a novel regulator of colitis.
资助项目MOST | National Natural Science Foundation of China (NSFC)[81900496];MOST | NSFC | NSFC-Zhejiang Joint Fund | | Natural Science Foundation of Zhejiang Province (ZJNSF)[LZ24H090003]
出版者SPRINGERNATURE
ISSN1469-221X
EISSN1469-3178
DOI10.1038/s44319-024-00276-6
页数19
WOS类目Biochemistry & Molecular Biology ; Cell Biology
WOS研究方向Biochemistry & Molecular Biology ; Cell Biology
WOS记录号WOS:001324538700003
收录类别PUBMED ; SCIE
URL查看原文
PubMed ID39333628
通讯作者地址[Wang, Xu]Wenzhou Med Univ, Oujiang Lab, Zhejiang Lab Regenerat Med Vis & Brain Hlth, Wenzhou 325035, Peoples R China. ; [Wang, Xu]Wenzhou Med Univ, Sch Pharmaceut Sci, Wenzhou 325035, Peoples R China. ; [Ruan, Jing]Wenzhou Med Univ, Affiliated Hosp 1, Dept Pathol, Wenzhou 325000, Peoples R China.
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/218993
专题药学院(分析测试中心)
附属第一医院
附属第一医院_病理科
其他_瓯江实验室
作者单位
1.Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health); School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, China.;
2.Department of Pharmacy, Yiwu Central Hospital, 322099, Yiwu, China.;
3.Department of Pathology, The First Affiliated Hospital, Wenzhou Medical University, 325000, Wenzhou, China.;
4.Institute for Molecular Medicine, Johannes Gutenberg University Mainz, 55131, Mainz, Germany.;
5.Department of Pathology, The First Affiliated Hospital, Wenzhou Medical University, 325000, Wenzhou, China. ruanjing850617@163.com.;
6.Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health); School of Pharmaceutical Sciences, Wenzhou Medical University, 325035, Wenzhou, China. sunrim@163.com.
第一作者单位药学院(分析测试中心);  瓯江实验室
通讯作者单位温州医科大学;  药学院(分析测试中心);  附属第一医院;  病理科
第一作者的第一单位药学院(分析测试中心)
推荐引用方式
GB/T 7714
Jiangyun Shen,Liyan Lou,Xue Du,et al. YOD1 sustains NOD2-mediated protective signaling in colitis by stabilizing RIPK2[J]. EMBO reports,2024.
APA Jiangyun Shen., Liyan Lou., Xue Du., Bincheng Zhou., Yanqi Xu., ... & Xu Wang. (2024). YOD1 sustains NOD2-mediated protective signaling in colitis by stabilizing RIPK2. EMBO reports.
MLA Jiangyun Shen,et al."YOD1 sustains NOD2-mediated protective signaling in colitis by stabilizing RIPK2".EMBO reports (2024).

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