MMP14 Antibody
- Known as:
- MMP14 Antibody
- Catalog number:
- 48-562
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MMP14 Antibody
Related genes to: MMP14 Antibody
- Gene:
- MMP14 NIH gene
- Name:
- matrix metallopeptidase 14
- Previous symbol:
- -
- Synonyms:
- MT1-MMP
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: MMP14 Antibody
Related articles to: MMP14 Antibody
- Matrix metalloproteinases (MMPs) play critical roles in wound repair, yet their context-dependent functions in diabetic wound healing remain elusive. In this study, we found that both the expression and activity of MMP14 were significantly elevated in diabetic foot ulcers (DFUs). Using animal models, we further revealed the dual roles of MMP14 in wound healing. In normal rats, inhibition of MMP14 delayed wound closure, confirming its supportive role in physiological tissue repair. In contrast, in diabetic rats, pathologically increased MMP14 levels impaired healing, whereas moderate inhibition significantly accelerated wound repair. Among the inhibitors tested, the selective MMP14 inhibitor NSC405020 produced the most favorable therapeutic effect in diabetic wounds, markedly enhancing healing rates and collagen deposition at a concentration of 1 mg/mL. Compared with the broad-spectrum MMP inhibitor ND336, NSC405020 demonstrated therapeutic safety and comparable efficacy without notable toxicity in a rat model. Collectively, these findings elucidate the context-dependent role of MMP14 in wound healing, suggesting that MMP14 may be a promising therapeutic target for diabetic wound healing. Therefore, our study provides a theoretical foundation for the development of effective and safe treatments for diabetic wound management. - Source: PubMed
Publication date: 2026/08/21
Zeng Gui-FengChen GuotianZhou ZhenChen Hui-GuangZhang Guo-PingZou Shui-LanYuan ZiyanPan de-HongZhou Hai-YangWang GuiqingZhang Da-WeiXia Xiaodan - T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by aberrant epigenetic regulation. Although SET domain-containing 5 (SETD5) is structurally classified as a member of the histone methyltransferase family, it lacks canonical methyltransferase activity and functions primarily through nonenzymatic mechanisms. While recognized as a modulator in normal hematopoiesis, the role of SETD5 in T-ALL remains undefined. Here, we show that SETD5 contributes to efficient T-ALL initiation and progression in the models examined. Using ICN1-driven murine T-ALL models (Vav-Cre;Setd5 and Mx1-Cre;Setd5), we show that genetic ablation of Setd5 impairs efficient leukemia initiation. In transplantation assays, Setd5 depletion reduces leukemia burden, prolongs survival, and impairs leukemic infiltration into the spleen, liver, and thymus. Mechanistically, transcriptomic profiling of Setd5-deficient CD3 T-ALL cells reveals selective repression of transcriptional programs governing cell migration, motility, and cytoskeletal organization. Key regulators of actin cytoskeleton remodeling and extracellular matrix interaction-including Plxnb2, Mmp14, Ceacam1, and Clstn1-are among the most downregulated genes, as validated by RT-qPCR. Furthermore, SETD5 knockdown in the human T-ALL cell lines Jurkat and MOLT-4 results in a marked reduction in proliferation and migration. Our findings demonstrate that SETD5 contributes to T-ALL progression by regulating transcriptional programs that contribute to leukemic cell migration and infiltration, suggesting that SETD5-associated transcriptional programs warrant further investigation as potential vulnerabilities in T-ALL. - Source: PubMed
Publication date: 2026/08/13
Hao MingyueBian YujieLi MengkeLiu TongLi HaoyuanCao MutianHe YifeiCong LizhenLing YuanyiGu ShilongLi WantingZhang MingyueYuan WeipingChu Yajing - Hypertensive retinopathy is a microvascular complication caused by systemic hypertension and can lead to severe visual impairment. At present, the molecular mechanisms of this disease remain incompletely understood, particularly the global expression profiles and regulatory networks of non-coding RNA (ncRNA). This study aims to comprehensively analyze the genome-wide differential expression profiles of messenger RNA (mRNA), microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) in retinal tissues from a spontaneously hypertensive rat (SHR) model of hypertensive retinopathy, and to observe transcriptomic changes after treatment with the calcium channel blocker lacidipine, thereby revealing their potential roles in disease pathogenesis and identifying possible therapeutic targets. - Source: PubMed
Shi WenXiao ShiyuanBu BingHuang TianxinJiang YiranJiang Wenmin - Alcohol consumption has been a risk factor for more than 200 diseases, including esophageal cancer. Cell communication network 1 (CCN1), a matricellular protein, is highly expressed in esophageal squamous cell carcinoma (ESCC) but is barely detectable in esophageal adenocarcinoma (EAC). Alcohol consumption has been identified as a major contributor to ESCC development, but its role in EAC is uncertain. This study examines the impact of acute (30 min) or prolonged (12 h) alcohol exposure (5, 100, and 500 mM) on CCN1 expression and function in esophageal epithelial cells, including normal (HEEC), ESCC (KYSE150 and KYSE410), and EAC (OE19 and OE33), in association with the activity of MMP2, MMP9, and MMP14. It was found that alcohol exposure promoted CCN1 expression in both normal and tumor cells but induced CCN1 cleavage exclusively in EAC cells, generating an 18-kDa fragment that promotes tumor growth. MMP9, which was active only in EAC cells, was found to mediate this cleavage. Forced activation of MMP9 in either normal or ESCC cells improved cell viability, whereas inhibition of MMP9 in EAC cells attenuated cell survival. Taken together, alcohol exposure promotes MMP9-mediated CCN1 cleavage in EAC, converting CCN1 from a pro-death to a pro-survival factor for EAC. This makes alcohol consumption a risk factor not only for ESCC development but also for EAC progression. A preprint can be found at d197for5662m48.cloudfront.net. - Source: PubMed
Publication date: 2026/08/05
Aladan WulaChi BaoxinChang ZhihengWang MizhuDang TongMeng XianmeiChai Jianyuan - Idiopathic pulmonary fibrosis(IPF) is a fatal interstitial lung disease with limited clinical therapeutic options. Traditional Chinese medicine formulas, characterized by multi-component, multi-target, and holistic regulatory properties, have shown unique potential in the prevention and treatment of IPF. Yangyin Yifei Tongluo Pills(YF) is a TCM formula with demonstrated clinical efficacy. However, its modern pharmacological mechanism against IPF remains to be systematically elucidated. In this study, ultra-high-performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry(UHPLC-Q Exactive Orbitrap-HRMS) was employed to identify the chemical constituents of YF. A total of 76 potential bioactive compounds were characterized, including flavonoids, phenylpropanoids and other chemicals. By integrating network pharmacology and bioinformatics analyses, drug-related targets, IPF-associated targets, differentially expressed genes, and WGCNA-derived key module genes were intersected, yielding 15 potential targets. Based on a systematic evaluation using nine machine learning algorithms, arginase 1(ARG1) and matrix metalloproteinase 14(MMP14) were identified as key core targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses indicated that these targets were mainly involved in inflammatory regulation, signal transduction, and extracellular matrix(ECM) remodeling, with significant enrichment in key signaling pathways such as the TNF signaling pathway. Immune microenvironment analysis revealed that the expression levels of ARG1 and MMP14 were closely associated with immune and stromal cell infiltration characteristics. Molecular docking demonstrated favorable binding affinities between ARG1/MMP14 and several core components, including miltirone, peimine, cryptotanshinone, and sec-O-glucosylhamaudol, while molecular dynamics simulations further confirmed the conformational stability of miltirone and sec-O-glucosylhamaudol, as core potential bioactive components, with the targets under dynamic conditions. Collectively, these findings suggest that YF may exert anti-IPF effects by targeting ARG1 and MMP14 through its core potential bioactive components, synergistically modulating key processes including the immune microenvironment, fibroblast activation, and extracellular matrix remodeling. By integrating LC-MS, bioinformatics, machine learning, immune infiltration analysis, molecular docking, and molecular dynamics simulation, this study systematically elucidates the multi-component and multi-target mechanisms of YF, providing new insights and a foundation for the intervention and treatment of IPF and the mechanistic study of TCM formulas. - Source: PubMed
Wen Ke-HanZhao QiGuo Ao-JieWu Zhi-ChaoXia Xiao-LinChen Le-leXu YongXiao Na