Mouse MMP14 ELISA Kit
- Known as:
- Mouse MMP14 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- orb56305
- Product Quantity:
- 96 well
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Mouse MMP14 ELISA Kit
Related genes to: Mouse MMP14 ELISA Kit
- 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 ELISA Kit
Related articles to: Mouse MMP14 ELISA Kit
- 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 - Bovine digital dermatitis (BDD) is an infectious disease in cattle associated with multiple Treponema species yet information on the immune responses of circulating immune cells to these pathogens are limited. In this study, we characterized the transcriptomic responses of bovine peripheral blood mononuclear cells (PBMCs) following stimulation with combined whole cell lysates derived from three BDD-associated Treponema species. PBMCs were stimulated for 12 h and differentially expressed genes between non-stimulated control and stimulated groups were identified. Functional enrichment of DEGs was assessed using Gene Ontology (GO). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed to provide a functional annotation of DEGs. A total of 3458 DEGs were identified, including 1770 upregulated and 1688 downregulated genes (BH-FDR adjusted p-value < 0.05). Notable upregulated genes included IFNγ, CXCL10, IL17F, IL1B, IL6, MMP9, and MMP14 linked to Th1 and Th17 responses, pro-inflammatory cytokine production and extracellular matrix (ECM) remodeling. In contrast, genes associated with antimicrobial activity, complement regulation, and immune modulation, such as LYZ, KLF4, CFD, and NR4A3, were markedly downregulated suggesting suppression of innate immune response and regulatory mechanisms potentially favoring a pro-inflammatory state in PBMCs. Enriched pathways included mitogen-activated protein kinase (MAPK) and tumor necrosis factor (TNF) signaling which could be a key driver in pro-inflammatory signaling and ECM processes. The enrichment of the NOD-like receptor pathway indicates that Treponema spp. whole cell lysates may influence inflammasome-associated and non-canonical inflammatory programs. Overall, this study provides valuable information for further exploration of host-pathogen interactions in BDD. - Source: PubMed
Publication date: 2026/05/07
Valete Edeneil JeromeEspiritu HectorCho Yong-Il - This study aimed to characterize large and small RNA transcriptomic changes in fibroid xenografts from mice treated with the TDO2 inhibitor 680C91 for two months and to validate selected findings using qRT-PCR, protein analyses, and in vitro fibroid explant models. Large RNA next-generation sequencing revealed that 680C91 induced broad transcriptomic alterations, with enrichment of pathways related to the extracellular space, RNA processing, PI3K/AKT signaling, and calcium signaling. Small RNA sequencing identified enrichment of pathways associated with PI3K/AKT signaling, proteoglycans in cancer, and interleukin signaling. Key differentially expressed genes were validated in xenografts and fibroid explants. Treatment with 680C91 significantly reduced the mRNA expression of VDR, MMP11, MMP14, COL11A1, CBX4, LINC02568, LINC01310, LINC02544, and LINC02182, while increasing miR-584-5p expression. These changes were consistently observed in fibroid explants treated with 680C91 for 48 hours. Corresponding decreases in protein levels of COL11A1, VDR, CBX4, MMP11, and MMP14 were also detected. Additionally, 680C91 inhibited AKT phosphorylation and reduced α-smooth muscle actin and vimentin expression. Importantly, all validated transcripts displayed expression patterns opposite to those observed in fibroid tissues compared with matched myometrium, with more pronounced effects in MED12-mutated tumors. These preclinical findings support TDO2 inhibition as a potential therapeutic strategy for uterine fibroids. - Source: PubMed
Publication date: 2026/05/11
Chuang Tsai-DerWiseman AbigailAlfaro GabrielaPejouhesh Jahromi SaynaPejouhesh Jahromi SepidehBaghdasarian DanielKhorram Omid - Diabetic kidney disease (DKD) is a leading microvascular complication of diabetes in which vascular smooth muscle cell (VSMC) senescence plays a pivotal pathogenic role. This study aimed to identify key genes regulating VSMC senescence in DKD through integrated bioinformatics and machine learning analysis, construct a diagnostic nomogram prediction model, screen candidate therapeutic compounds, and validate findings experimentally. - Source: PubMed
Publication date: 2026/05/01
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