MMP14 Monoclonal Antibody (C_term)
- Known as:
- MMP14 Monoclonal Antibody (C_term)
- Catalog number:
- AM1832a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- MMP14 Monoclonal Antibody (C_term)
Related genes to: MMP14 Monoclonal Antibody (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: MMP14 Monoclonal Antibody (C_term)
Related articles to: MMP14 Monoclonal Antibody (C_term)
- 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 - Vascular smooth muscle cells (VSMCs) dedifferentiation is a key driver of peripheral artery disease (PAD), a common complication of atherosclerosis. Although matrix metallopeptidase 14 (MMP14) has been implicated in promoting VSMC dedifferentiation, the underlying mechanisms remain incompletely defined. Here, we demonstrate that MMP14 expression is markedly increased in PAD plaques, accompanied by elevated platelet-derived growth factor receptor-β (PDGFRβ) and reduced low-density lipoprotein receptor-related protein 6 (LRP6) levels, predominantly within VSMCs, compared with plaque-free arterial segments. Mechanistically, MMP14 selectively promoted LRP6 shedding without affecting LRP5 in VSMCs. Genetic or pharmacological inhibition of MMP14 increased LRP6 abundance, reduced PDGFRβ and SP1 expression, attenuated ERK phosphorylation, and suppressed VSMC proliferation and migration. In contrast, MMP14 overexpression produced opposite effects. Collectively, these findings indicate that MMP14 enhances VSMC proliferation and migration through modulation of the LRP6-PDGFRβ signaling axis. - Source: PubMed
Publication date: 2026/05/14
Chen Hui-GuangGao DiZeng Gui-FengZhang Guo-PingYuan Zi-YanPan De-HongQin Yi-KunLv Zhong-YuanTan Xiao-BoChen Guo-TianWang Gui-QingZhang Da-WeiXia Xiao-Dan - Despite the proliferation of prognostic gene signatures for glioma, clinical translation remains stalled by poor reproducibility and overfitting. In this study, we address this stability crisis by developing a robust "Dual-Signature Framework" using stability selection-a rigorous resampling method-rather than standard regression. Analyzing RNA-seq data from 1351 patients across the TCGA (n = 694) and CGGA (n = 657) cohorts, we constructed two distinct models. The primary 20-gene "Data-Driven" signature achieved superior predictive accuracy (C-index: 0.7392), significantly outperforming 14 published benchmark models and the current best single-gene predictor (HOXA5). In parallel, we derived a 7-gene "Biology-Driven" signature (including HOXA5, CHI3L1, MMP14) that retained 98% of the predictive power (C-index: 0.7252) while prioritizing mechanistic interpretability. Both models successfully stratified patients into distinct risk groups with high statistical significance (Log-rank p < 0.001) in external validation. Comprehensive subgroup analyses across 19 clinical and molecular subgroups demonstrated robust performance (C-index range: 0.59-0.85), with extended calibration analysis confirming excellent probability estimation (Brier score 0.20 for 5-year predictions). By integrating stability-driven feature selection with biological pathway constraints, this study provides a reproducible, high-performance alternative to unstable "black box" models, offering a translation-ready tool for personalized glioma risk assessment. - Source: PubMed
Publication date: 2026/05/12
D'Costa Romeo MaclineIslam Md ShafiqulIslam Md Masudul - A high-fat, high-cholesterol diet (HFHCD) has a lipotoxic effect on the heart. It not only leads to the development of atherosclerosis but also influences the extracellular matrix within the heart. The aim of the study was to investigate the effect of HFHCD on matrix metalloproteinases MMP-2, MMP-9, MMP-13, and MMP-14 expression in both the cardiac tissue and plasma of ApoE (-/-) mice and on mRNA expression of c-Jun and TGF-β in the cardiac tissue of both ApoE (-/-) mice and wild-type C57BL/6J mice. The study was carried out on two groups of ApoE (-/-) mice: (1) mice from 10 weeks of age that were kept on a HFHCD ( = 10) for the following 14 weeks; (2) control mice (NFD, = 10) that were kept on a standard, normal-fat diet for the same time as the HFHCD. Additionally, 10 wild-type (WT) mice on a standard, normal-fat diet were also included in the study for mRNA analysis of c-Jun and TGF-β. Atherosclerotic plaque, intima, and media dimensions were assessed in the aortas of the ApoE (-/-) mice by histopathology. Concentrations of MMP-2, MMP-9, MMP-13, and MMP-14 were assessed by ELISA both in cardiac tissue and in the plasma of the ApoE (-/-) HFHCD and ApoE (-/-) NFD mice, while the mRNA expression of c-Jun and TGF-β was assessed by RT-PCR in both the ApoE (-/-) and WT groups. The results demonstrate a significantly increased MMP-9 concentration in the cardiac tissue of the HFHCD mice compared to the NFD mice (2.83 ng/mL vs. 1.91 ng/mL, = 0.006), and a moderate correlation between the cardiac and plasmatic MMP-9 in ApoE (-/-) mice (r = 0.492, = 0.0398). Moreover, although the mRNA expression of c-Jun and TGF-β did not differ between NFD and HFHCD ApoE (-/-) mice, the c-Jun expression was significantly elevated in the WT group compared with both ApoE (-/-) groups. The study demonstrated that a high-fat, high-cholesterol diet increases MMP-9 concentration in cardiac tissue, which might reflect its influence on the extracellular matrix within the heart. - Source: PubMed
Publication date: 2026/04/27
Kowara MichałCzarzasta KatarzynaJędrzejewski MichałKoperski ŁukaszSegiet-Święcicka AgnieszkaWrzesień RobertKuch MarekCudnoch-Jędrzejewska Agnieszka