MMP14 antibody
- Known as:
- MMP14 (anti-)
- Catalog number:
- orb36366
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- 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
- Approximately 10% of glioblastomas harbor targetable genomic fusions. participates in a variety of fusion events that drive tumorigenesis. Two previous reports have described fusions in adult glioblastoma patients with poor survival. - Source: PubMed
Publication date: 2026/08/20
Sadanandappa Madhumala KKarbhari NishikaKnowles BrizhaPalisoul Scott MHughes Edward GTafe Laura JZanazzi George JLin Chun-ChiehHong Jennifer - Dedifferentiated liposarcoma (DDLPS) is an aggressive mesenchymal malignancy coexisting with a low grade well-differentiated component. Pathways implicated in liposarcoma growth and dedifferentiation are promoted by heparan sulfate (HS) proteoglycans (HSPG) and their modifying enzymes including heparanase. HSPGs serve as co-receptors enhancing tyrosine kinase signaling and tumor aggressiveness. Targeting these interactions bears promise in attenuating liposarcoma growth. We employed an investigational HS mimetic, the non-anticoagulant heparin CX-01 (dociparstat), to assess its HS competition impact on deregulated adipogenic differentiation and growth of human DDLPS cell lines and patient-derived xenografts (PDXs). Remarkably, CX-01 reduced colony formation and invasive capacities of DDLPS cell lines, inducing cytoskeleton remodeling, lipid accumulation and reactivation of adipogenic program. Mechanistic studies into the anti-DDLPS activity of CX-01 unveiled Syndecan 1 (SDC1)/heparanase system and receptor tyrosine kinase-AKT signaling as targets of cell growth inhibition and induction of differentiation. CX-01 treatment of mice harboring DDLPS PDXs attenuated tumor growth, enhanced lipid content and consistently altered the transcriptome, modulating pathways associated with tumor dedifferentiation (adipogenesis and fatty acid metabolism) and tumor-microenvironment interaction (TGFβ signaling, inflammatory response). In two independent cohorts of DDLPS patients, genes downregulated in CX-01-treated PDXs (SDC1, TIMP1, FN1, COL5A1, and MMP14), were found preeminently expressed in the dedifferentiated, compared to the well-differentiated tumor component and normal fat. This suggests a role for these genes in disease progression. Collectively, this study demonstrates the remarkable potential of HS competition to simultaneously block multiple anti-adipogenic players representing metabolic vulnerabilities, and to promote a differentiated tumor phenotype markedly less aggressive. - Source: PubMed
Publication date: 2026/08/11
Lanzi CinziaFavini EnricaDal Bo LauraTortoreto MonicaPercio StefanoZuco ValentinaDagrada Gian PaoloBrich SilviaCollini PaolaDe Cecco LorisCallegaro DarioSanfilippo RobertaGronchi AlessandroZaffaroni NadiaAssaraf Yehuda GPasquali SandroCassinelli Giuliana - Vitamin D has been reported to act as a tissue-protective regulator by suppressing Matrix Metalloproteinases (MMPs) and upregulating Tissue Inhibitors of Metalloproteinases (TIMPs), though changes may be body mass index (BMI)-dependent; however, the relationship between vitamin D metabolism and matrix remodeling pathways in Polyendocrine Metabolic Ovarian Syndrome (PMOS) remains poorly understood. In women with PMOS ( = 28) and controls ( = 28), 12 MMPs and 3 TIMPs were determined by Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement and correlated to 25-hydroxyvitamin D (25(OH)D) and its metabolites (active 1,25-dihydroxyvitamin D (1,25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)D)) measured by gold standard isotope-dilution liquid chromatography tandem mass spectrometry. Insulin resistance and systemic inflammation (normal C-reactive protein) were comparable between PMOS and control women, though PMOS had higher free androgen index and anti-Mullerian hormone levels. Vitamin D and its metabolites did not differ between groups. Only MMP16 was lower in PMOS than controls (549.6 ± 58.3 vs. 678.0 ± 304.1 Relative Fluorescent Units, = 0.037) but did not pass the false discovery rate. In women with PMOS, 25(OH)D and 24,25(OH)D demonstrated significant inverse correlations with TIMP3 (r = -0.60, = 0.005 and r = -0.58, = 0.007, respectively). Multivariable regression confirmed independent inverse associations between TIMP3 and both 25(OH)D (β = -51.1, = 0.031) and 24,25(OH)D (β = -858.7, = 0.028) after adjustment for age, body mass index and Homeostatic Model Assessment-Insulin Resistance, and the association remained stable following bootstrap internal validation. Additional moderate associations were observed between vitamin D metabolites and membrane-type MMPs (MMP14, MMP16, MMP17). Exploratory analyses suggested potential inverse associations between vitamin D metabolites and TIMP3, together with weaker associations involving MMP14, MMP16 and MMP17, suggesting the novel hypothesis that vitamin D may influence extracellular matrix remodeling and ovarian stromal biology through regulation of TIMP3-dependent pathways independently of obesity and insulin resistance, rather than through MMPs directly. - Source: PubMed
Publication date: 2026/07/24
Zainalabedin MashaelSmahi NoraSathyapalan ThozhukatButler Alexandra EAtkin Stephen L - Osteosarcoma (OS) is the most common human primary bone cancer, primarily affecting children and young adults. While the survival rate of patients diagnosed with localized OS is ∼65%, this decreases to ∼20% for patients with metastatic disease, and recurrent disease remains largely incurable. Therefore, identifying new therapeutic strategies is urgently needed for metastatic and refractory OS. This study analyzes the surfaceomes and global proteomes of 22 unique OS patient-derived xenografts (PDXs) using mass spectrometry to identify surface proteins for potential immunotherapeutic targeting. Both methods identify known OS-associated surface candidates including LRRC15, MMP14, MRC2, and CADM1, and several poorly characterized targets, including ROR2 and TMEM119. Both ROR2 and TMEM119 display robust expression in OS tissues but only limited or no expression in normal pediatric tissues, and loss of both targets reduces the migration of OS cells. These data provide a resource of surface proteins as potential immunotherapeutic targets in OS. - Source: PubMed
Publication date: 2026/08/26
Mooney BrianChu XiaojieNegri Gian LucaLizardo Michael MSong HarleyMarsh AlisonDelaidelli AlbertoHuang Yue ZRouleau MelanieSpencer Sandra EShraim RawanHamilton Amber KMagesh SruthiZhang WendongBudhathoki YogeshCannon Matthew VRoberts RyanGorlick RichardSweet-Cordero AlejandroDiskin Sharon JMaris John MLi WeiMorin Gregg BSorensen Poul H - 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