MMP17

更新于：2025-05-07

基本信息

别名

matrix metallopeptidase 17、matrix metallopeptidase 17 (membrane-inserted)、matrix metalloproteinase 17 (membrane-inserted)

+ [9]

简介

Endopeptidase that degrades various components of the extracellular matrix, such as fibrin. May be involved in the activation of membrane-bound precursors of growth factors or inflammatory mediators, such as tumor necrosis factor-alpha. May also be involved in tumoral process. Cleaves pro-TNF-alpha at the '74-Ala-|-Gln-75' site. Not obvious if able to proteolytically activate progelatinase A. Does not hydrolyze collagen types I, II, III, IV and V, gelatin, fibronectin, laminin, decorin nor alpha1-antitrypsin.

关联

项与 MMP17 相关的药物

TIMP-4 (Transgene)

靶点

MMP17

作用机制

MMP17刺激剂

在研机构-

原研机构

Human Genome Sciences, Inc.

在研适应症-

非在研适应症

血管再狭窄

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 MMP17 相关的临床结果

登录后查看更多信息

100 项与 MMP17 相关的转化医学

登录后查看更多信息

0 项与 MMP17 相关的专利（医药）

登录后查看更多信息

128

项与 MMP17 相关的文献（医药）

2024-08-01·International Journal of Obesity

An epigenome-wide association study of waist circumference in Chinese monozygotic twins

Article

作者: Duan, Haiping ; Xing, Fangjie ; Tian, Huimin ; Lv, Bosen ; Wu, Yili ; Tian, Xiaocao ; Xu, Chunsheng ; Zhang, Dongfeng ; Han, Fulei ; Wang, Weijing ; Wu, Yan

OBJECTIVESCentral obesity poses significant health risks because it increases susceptibility to multiple chronic diseases. Epigenetic features such as DNA methylation may be associated with specific obesity traits, which could help us understand how genetic and environmental factors interact to influence the development of obesity. This study aims to identify DNA methylation sites associated with the waist circumference (WC) in Northern Han Chinese population, and to elucidate potential causal relationships.METHODSA total of 59 pairs of WC discordant monozygotic twins (ΔWC >0) were selected from the Qingdao Twin Registry in China. Generalized estimated equation model was employed to estimate the methylation levels of CpG sites on WC. Causal relationships between methylation and WC were assessed through the examination of family confounding factors using FAmiliaL CONfounding (ICE FALCON). Additionally, the findings of the epigenome-wide analysis were corroborated in the validation stage.RESULTSWe identified 26 CpG sites with differential methylation reached false discovery rate (FDR) < 0.05 and 22 differentially methylated regions (slk-corrected p < 0.05) strongly linked to WC. These findings provided annotations for 26 genes, with notable emphasis on MMP17, ITGA11, COL23A1, TFPI, A2ML1-AS1, MRGPRE, C2orf82, and NINJ2. ICE FALCON analysis indicated the DNA methylation of ITGA11 and TFPI had a causal effect on WC and vice versa (p < 0.05). Subsequent validation analysis successfully replicated 10 (p < 0.05) out of the 26 identified sites.CONCLUSIONSOur research has ascertained an association between specific epigenetic variations and WC in the Northern Han Chinese population. These DNA methylation features can offer fresh insights into the epigenetic regulation of obesity and WC as well as hints to plausible biological mechanisms.

2024-07-01·Biochemistry and Biophysics Reports

SH3GL2 and MMP17 as lung adenocarcinoma biomarkers: a machine-learning based approach.

Article

作者: Yu, Shilong ; Tian, Zengjian ; Liu, Qilun ; Cai, Ruizhi ; Zhu, Yongzhao ; Zhang, Yinghui

ObjectiveUsing bioinformatics machine learning methods, our research aims to identify the potential key genes associated with Lung adenocarcinoma (LUAD).MethodsWe obtained two gene expression profiling microarrays (GSE68571 and GSE74706) from the public Gene Expression Omnibus (GEO) database at the National Centre for Biotechnology Information (NCBI). The purpose was to identify Differentially Expressed Genes (DEGs) between the lung adenocarcinoma group and the healthy control group. The limma R package in R was utilized for this analysis. For the differential gene diagnosis of lung adenocarcinoma, we employed the least absolute shrinkage and selection operator (LASSO) regression and SVM-RFE screening crossover. To evaluate the performance, ROC curves were plotted. We performed immuno-infiltration analysis using CIBERSORT. Finally, we validated the key genes through qRT-PCR and Western-blot verification, then downregulated MMP17 gene expression, upregulated SH3GL2 gene expression, and performed CCK8 experiments.ResultsA total of 32 Differentially Expressed Genes (DEGs) were identified. Two diagnostic marker genes, SH3GL2 and MMP17, were selected by employing LASSO and SVM-RFE machine learning methods. In Lung adenocarcinoma cells, the expression of MMP17 was observed to be elevated compared to normal lung epithelial cells in the control group (P < 0.05). In contrast, a down-regulation of SH3GL2 was found in Lung adenocarcinoma cells (P < 0.05). Finally, we downregulated MMP17 and upregulated SH3GL2 gene expression, then the CCK8 showed that the proliferation of both lung cancer cells was inhibited.ConclusionSH3GL2 and MMP17 are expected to be potential biomarkers for Lung adenocarcinoma.

2024-04-01·Arteriosclerosis, Thrombosis, and Vascular Biology

Single-Cell Transcriptome Reveals Potential Mechanisms for Coronary Artery Lesions in Kawasaki Disease

Article

作者: Wang, Hongmao ; Chen, Yeshi ; Li, Xiaohui ; Sun, Rui ; Zheng, Yang ; Yang, Minna ; Zhang, Mingming

BACKGROUND:Coronary artery lesions (CALs) are the most common and major complication of Kawasaki disease (KD) in developed countries. However, the underlying immunologic mechanisms of CAL development in KD remain unclear.METHODS:Here, we conducted single-cell transcriptome analyses of 212 210 peripheral blood mononuclear cells collected from a cross-sectional cohort of 16 children, including 4 patients with KD with CALs, 5 patients with KD without CALs, 4 healthy controls, and 3 febrile controls.RESULTS: KD altered the proportion of peripheral blood mononuclear cells, including an increasing trend in inflammatory cells (megakaryocytes and monocytes) and a decreasing trend in lymphocytes (eg, CD4 + T, CD8 + T, mucosal-associated invariant T, natural killer, and γδ T cells), highlighting the potential presence of lymphopenia phenomenon in KD. Our data indicated the presence of inflammatory cytokine storm in patients with KD with CALs, caused by systemic upregulation of TNFSF13B (tumor necrosis factor superfamily member 13b), CXCL16 (C-X-C motif chemokine ligand 16), TNFSF10 (tumor necrosis factor superfamily member 10), and IL1RN (interleukin 1 receptor antagonist), mainly produced by monocytes (especially for the Mono_CD14-CD16 cluster) and megakaryocytes. We also found that myeloid cells of patients with KD, particularly in those with CALs, might play a role in vascular injury (eg, increased MMP [matrix metalloproteinase] 9, MMP17, and MMP25) and immune cell recruitment. The immune landscape of patients with KD with CALs was featured by lower exhaustion levels in natural killer cells, a high cytotoxic state in the CD8_Pro cluster, and activation of the complement system in monocytes. Additionally, the activation of B cells was more pronounced in the early stage of KD. CONCLUSIONS:Collectively, this study provides a comprehensive understanding of the roles of various immune cells and inflammatory cytokine storms in the development of CALs in KD and offers a valuable resource for identifying novel therapeutic targets for patients with KD with CALs.