MMP14 (Cleaved-Tyr112) antibody
- Known as:
- MMP14 (Cleaved-Tyr112) (anti-)
- Catalog number:
- orb126637
- Product Quantity:
- 5 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MMP14 (Cleaved-Tyr112) antibody
Related genes to: MMP14 (Cleaved-Tyr112) 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 (Cleaved-Tyr112) antibody
Related articles to: MMP14 (Cleaved-Tyr112) antibody
- Vascular calcification is an actively regulated process driven by vascular smooth muscle cell (VSMC) osteogenic reprogramming and promoted by oxidative stress and extracellular matrix remodeling. We investigated whether the novel histone deacetylase inhibitor YAK577 mitigates calcification by modulating an MMP14-NOX2/ROS-associated pathway in calcification medium (CM)-treated VSMCs and a vitamin D-induced arterial calcification model in 8-week-old male C57BL/6N mice. Calcification was assessed by Alizarin Red S/von Kossa staining and calcium quantification; osteogenic markers (BMP2, RUNX2, MSX2) and MMPs were examined by qRT-PCR and immunoblotting; intracellular ROS was measured by DHE staining with N-acetylcysteine as an antioxidant control; and MMP14 was manipulated by siRNA knockdown or plasmid overexpression. YAK577 was non-cytotoxic at effective concentrations and reduced CM-induced calcium deposition and osteogenic marker expression. YAK577 reduced MMP14 expression and suppressed CM-induced NOX2/p47phox activation and ROS accumulation, while GSK2795039 attenuated CM-induced DHE fluorescence. MMP14 silencing attenuated, whereas MMP14 overexpression enhanced, osteogenic signaling and increased NOX2. In vivo, YAK577 reduced vitamin D-induced aortic calcium burden, histological calcification, and the expression of MMP14, NOX2, and osteogenic markers. These data support a working model in which YAK577 alleviates vascular calcification, at least in part, by suppressing an MMP14-associated NOX2/p47phox-ROS axis. - Source: PubMed
Publication date: 2026/05/10
Zhou HongyanKee Hae JinJeong Seong MinBai LiyanWan LeKim Seong HoonLee Seung HunKurz ThomasSim Doo SunJeong Myung HoHong Young Joon - Periodontitis represents a chronic inflammatory disease resulting from the interaction between plaque-associated microorganisms and the host immune response. PANoptosis, a newly recognized programmed cell death, is linked to multiple inflammatory disorders. However, its role in periodontitis pathogenesis and diagnostic potential remains unclear. This study aimed to identify key PANoptosis-related biomarkers in periodontitis using bioinformatics analysis followed by experimental verification. - Source: PubMed
Publication date: 2026/05/15
Xi HualeiXu WanqiuLin SongYao LihongPiao GuiyanLiu YingGuo JinrongWang ShuminXie JiaxinWang Xiumei - Chronic periodontitis (CP) and postmenopausal osteoporosis (PMOP) are prevalent chronic inflammatory diseases characterized by bone resorption; however, the shared molecular mechanisms between them remain unclear. Hub genes associated with CP and PMOP were identified through bioinformatics analysis. Lipopolysaccharide (LPS)-stimulated MC3T3-E1 osteoblasts were used to establish an in vitro model, followed by lentiviral-mediated matrix metalloproteinase 14 (MMP14) knockdown. Cell viability and apoptosis were assessed using the Cell Counting Kit-8 assay and flow cytometry, respectively. Levels of inflammatory cytokines and oxidative stress markers were measured by enzyme-linked immunosorbent assay. Intracellular ROS were detected using 2',7'-dichlorodihydrofluorescein diacetate fluorescence staining. Western blot analysis was performed to assess the expression of osteoclast-related markers. The involvement of the JAK2/STAT3 pathway was assessed using the JAK2 agonist RO8191 and inhibitor AG490. PDGFRB, MMP14, VWF, PECAM1, FLT1, and CXCR4 were identified as hub genes and were all upregulated in LPS-stimulated MC3T3-E1 osteoblasts. Silencing MMP14 improved cell viability and reduced apoptosis, inflammatory cytokine release (TNF-α, IL-1β, and IL-6), oxidative stress markers (MDA and ROS), and osteoclast-associated markers (CTX-I, TRAP, and Cathepsin K), while restoring SOD activity. Mechanistically, MMP14 silencing decreased the phosphorylation levels of JAK2 and STAT3. The protective phenotype caused by MMP14 silencing was significantly abolished by RO8191 but mimicked by treatment with AG490. MMP14 may represent a potential molecular link between CP-associated bone loss and PMOP. Modulation of the MMP14-JAK2/STAT3 signaling axis may represent a promising research direction for inflammation-related bone loss. - Source: PubMed
Jiang XiliangJia WeiqiMa QinciFan WanpengLuo Shigao - Developmental dysplasia of the hip (DDH) is a common pediatric orthopedic disorder that predisposes affected children to early-onset osteoarthritis (OA), yet the cellular heterogeneity and fibrotic remodeling of acetabular cartilage are poorly understood. - Source: PubMed
Publication date: 2026/04/28
Nijiati YaxierSong JunHuang PengLin ZichenPei YingzhiNing Bo - Skin cancer, including basal cell carcinoma, squamous cell carcinoma, and melanoma, is one of the most common cancers worldwide. Matrix metalloproteinases are zinc-dependent proteolytic enzymes that play a crucial role in tumor invasion and angiogenesis by degrading the extracellular matrix. This study aims to analyze the specific expression of three matrix metalloproteinases (MMP-3, MMP-9, and MMP-14) to better understand the molecular mechanisms underlying the invasiveness of different skin cancer subtypes. - Source: PubMed
Publication date: 2026/05/04
Spatola Giovanni FrancescoPitruzzella AlessandroListro Antonino GioacchinoValenti CarlaScalisi MariaelenaMilia FedericaListro PaoloZingales FlaviaFerranti Giulio MariaListro MartaBelmonte BeatricePicone DomizianaIntili GiorgiaUzzo Maria Laura