Mouse Mmp14 (C-term)
- Known as:
- Mouse Mmp14 (C-terminus)
- Catalog number:
- AP19644b-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Mouse Mmp14 (C-term)
Related genes to: Mouse Mmp14 (C-term)
- 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: Mouse Mmp14 (C-term)
Related articles to: Mouse Mmp14 (C-term)
- 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 - Connective tissue remodeling is vital for organ development and tissue stability. Matrix metalloproteinases (MMPs), especially MMP14 and MMP13, are important collagenases that break down interstitial collagen in bone and skin. In mice, the loss of MMP14 results in perinatal death and severe skeletal defects, whereas Mmp13 deficiency causes transient bone defects that later resolve. Despite abundant dermal collagen, single knockouts usually do not display defects in skin formation, likely due to compensatory mechanisms. To examine their combined roles, mice lacking both enzymes were generated. These double-knockout mice were viable at birth but rapidly developed severe symptoms resembling Mmp14 deficiency, including growth retardation, wasting, and death within three weeks. Surprisingly, skin structure remained largely normal, aside from early subcutaneous fat loss also observed in Mmp14-deficient mice, indicating that neither enzyme is essential for early dermal remodeling. In contrast, skeletal defects worsened, showing shortened long bones, delayed primary ossification, impaired collagen type I breakdown, and reduced vascular invasion. These findings indicate that MMP13 partly compensates for MMP14 during bone development, while both enzymes are unnecessary for postnatal dermal collagen remodeling. Since MMP mutations are linked to human skeletal dysplasia, fibrosis, and wound-healing issues, these results underscore the distinct roles of MMP14 and MMP13 in collagen turnover and highlight their potential importance in human bone and connective tissue disorders. - Source: PubMed
Publication date: 2026/05/15
Bouriette BirgitGaessler LucaZamek JanSteinkamp JoyHuesgen PitterBrachvogel BentMauch CorneliaZigrino Paola - Chronic biliary injury drives liver fibrosis, yet mechanisms governing injury resolution and hepatocyte regeneration remain unclear. Periplakin (PPL), a cholangiocyte-enriched cytoskeletal linker, is upregulated during biliary injury, but its functional contribution to fibrosis and repair has not been defined. - Source: PubMed
Xu MeiyiningHuang YunJiang KefengZhang LichaoHuang WanxianShen JiaLei JunxiaHuang YanSun XiWu Zhongdao