MATN3 antibody
- Known as:
- MATN3 (anti-)
- Catalog number:
- orb75182
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MATN3 antibody
Related genes to: MATN3 antibody
- Gene:
- MATN3 NIH gene
- Name:
- matrilin 3
- Previous symbol:
- -
- Synonyms:
- EDM5, HOA
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-29
- Date modifiied:
- 2016-10-05
Related products to: MATN3 antibody
Related articles to: MATN3 antibody
- Triple-negative breast cancer (TNBC) remains a major cause of cancer mortality due to its aggressive behavior, metabolic adaptability, and high therapeutic resistance. Extracellular vesicles (EVs) within the tumor microenvironment contribute to tumor progression and metastasis by transferring pro-tumorigenic cargo. While conventional Tumor Treating Fields use high-frequency alternating fields to disrupt mitosis, low-energy triple-frequency bioelectromagnetic approaches remain poorly characterized. We evaluated a device-drug strategy combining triple-frequency low-intensity electromagnetic stimulation (EMS2: 396 Hz, 285 Hz, 528 Hz) with the pleiotropic drug Fingolimod (FTY720). Treatments were tested in MDA-MB-231 and ARM-G breast cancer cells, with Paclitaxel as a positive control. Cell proliferation was assessed by MTS assay, and extracellular vesicles were isolated following individual and combination treatments. Quantitative LC-MS/MS proteomics was used to characterize treatment-induced changes in EVs cargo. EMS2 reduced proliferation in both cell lines and produced morphological changes consistent with altered cell-cycle progression. EMS2 alone triggered adaptive metabolic responses, whereas combination with Fingolimod suppressed these compensatory signatures. EVs proteomics revealed combination-specific alterations associated with mitochondrial stress, ER stress, NF-κB suppression, and autophagy-associated pathways. The combination also reduced levels of metastasis- and stroma-associated proteins, including Mitogen-Activated Protein Kinase 12 (MAPK12) and collagen-associated ECM components (Collagen Type I Alpha 1 Chain (COL1A1), Collagen Type VI Alpha 1 Chain (COL6A1), Collagen Type VI Alpha 3 Chain (COL6A3), and Matrilin 3 (MATN3)) in EVs. Bliss independence analysis identified a subset of metastasis-associated proteins suppressed in EVs beyond the level predicted by an additive model, an exploratory finding that will require further validation with dose-response and functional assays. Combined triple-frequency EMS2 and Fingolimod treatment altered the extracellular vesicle proteome, inducing signatures consistent with mitochondrial and endoplasmic reticulum stress, metabolic disruption, and reduced levels of metastasis-associated and stromal/ECM remodeling proteins, along with reduced proliferation. These findings suggest a coordinated anti-cancer effect of this tunable device-drug strategy, warranting further functional and in vivo validation to confirm therapeutic potential. - Source: PubMed
Publication date: 2026/09/04
Haroutunian GregDaniels LawrenceTsaghikian AshotZhao CaifengZavras PhaedonMarukian SvetlanaZheng HaiyanMosoian Arevik - Differentiating bipolar disorder (BD) from major depressive disorder (MDD) remains a critical unmet need in psychiatry due to overlapping clinical presentations and the absence of reliable biological markers. In this study, we assessed the capacity of multivariate machine learning models to accurately differentiate BD from MDD with melancholic features using plasma proteomic profiles obtained via Proximity Extension Assay (PEA) technology. A total of 67 participants were included (23 BD, 20 MDD, and 24 HC), and plasma protein expression was assessed using the Olink Target 96 Neurology panel. Differential proteomic analysis revealed distinct disorder-specific expression patterns, identifying 21 differentially expressed proteins in BD versus MDD, 18 in BD versus healthy controls, and 7 in MDD versus healthy controls. Using a stepwise feature reduction strategy, machine learning models were trained on three feature sets comprising all proteins, the top 20 most informative proteins, and the top 5 most beneficial proteins, and evaluated across BD-MDD, BD-HC, and MDD-HC classification tasks using five algorithms. For BD-MDD discrimination, the Random Forest model achieved the highest performance when trained on the top 5 protein set (LXN, HAGH, MATN3, PLXNB1, and CTSC), yielding an AUC of 0.905, with similarly strong performance observed using the top 20 protein set. Feature importance analysis highlighted proteins involved in neurodevelopmental processes, immune regulation, and extracellular matrix organization. Overall, these findings demonstrate that integrating plasma proteomics with machine learning enables robust differentiation between BD and MDD with melancholic features, supporting the development of scalable and biologically informed diagnostic tools for precision psychiatry. - Source: PubMed
Publication date: 2026/09/09
Karacicek BilgeOzturk BilgesuArioz Burak IHok-A-Hin Yanaika SCavusoglu BerrinVerim BurcuBalaç SinemBabalıoğlu Reyhan NurGurkas SenaDaglar Zeynep GulCeylan DenizBora EmreTeunissen Charlotte EGenc SerminKeskinoglu Pembe - Intervertebral disc degeneration (IVDD) is a major cause and independent risk factor for low back pain. This study aims to explore the molecular mechanisms underlying IVDD and provide new ideas for targeted treatment. Cellular senescence is a key pathological event in IVDD, but its upstream regulatory network in nucleus pulposus cells (NPCs) remains unclear. This study found that MATN3 protein expression decreased significantly during IVDD, and its level was closely associated with NPC senescence. Functionality experiment data show that overexpression of MATN3 can effectively inhibits NPC senescence in vitro and delays the pathological progression of IVDD in a rat tail puncture model. Interestingly, no significant difference was observed in MATN3 at the mRNA level. Mechanistically, immunoprecipitation-mass spectrometry and co-immunoprecipitation identified USP5 as a direct interacting protein of MATN3, which it stabilized via deubiquitination, and functional rescue experiments confirmed that USP5 alleviated NPC senescence by upregulating MATN3. In conclusion, this study clarifies the molecular mechanism by which the USP5/MATN3 axis regulates cellular senescence and affects IVDD progression, opening up new potential targets for the intervention strategy of IVDD. - Source: PubMed
Publication date: 2026/07/17
Fan ChunyangXia JiechaoZhang YaoZhao JianbingQin WanjinZhang JianLing XuweiWu XiexingGeng DechunMao Haiqing - Gastric cancer (GC)-derived exosomes (Exos) have been identified to facilitate GC progression by inducing M2 macrophage polarization. This study investigated the biological function of exosomal matrilin-3 (MATN3) in M2 macrophage polarisation during GC development and its underlying mechanism. Exos were isolated from GC cells and then co-cultured with THP-1-derived macrophages. Macrophage polarisation was evaluated by measuring the levels of M1/M2 macrophage markers. Target molecule expression was evaluated by RT-qPCR, Western blotting and immunohistochemical staining. LC3II expression and the co-localisation of MATN3 and epidermal growth factor receptor (EGFR) were determined by immunofluorescent staining. In vivo growth of GC cells was assessed in a xenograft mouse model. Molecular mechanisms were analysed by Co-IP, ChIP, dual-luciferase reporter assay and ubiquitination assay. MATN3 was highly expressed in GC and its high expression was negatively associated with the overall survival and M1 macrophage marker expression of GC patients. The in vitro experiments validated that MATN3 was secreted by GC-Exos, which promoted M2 macrophage polarisation via autophagy activation. In addition, exosomal MATN3 contributed to in vivo growth of GC cells via promoting M2 macrophage infiltration. Mechanistically, MATN3 interacted with EGFR to enhance its protein stability, which activated Ets-like protein-1 (ELK1) and consequently promoted ATG12-mediated autophagy. Activation of the EGFR/ELK1 pathway abolished exosomal MATN3 silencing-mediated inhibitory effect on autophagy and M2 macrophage polarisation. GC-derived exosomal MATN3 exerted an oncogenic role by inducing M2 macrophage polarisation via activation of the EGFR/ELK1/ATG12 axis-mediated autophagy, which provides potential therapeutic targets for GC. - Source: PubMed
Publication date: 2026/05/20
Zhao QianwenLiu ShanshanShe XinMa ShiyueTang HuiPeng DanliGuo Haonan - Multiple epiphyseal dysplasia (MED) is a clinically and genetically heterogeneous group of disorders characterized by a waddling gait, joint pain, and early-onset osteoarthritis. The aim of this study was to compare the genetic characteristics and long-term clinical follow-up findings of 22 patients with MED from 17 unrelated families. Molecular diagnosis was performed using clinical exome analysis and exome sequencing. Seventeen children were followed for a median of 5.5 years. Eighteen disease-related variants were identified: 47% in , 11.8% each in and in a monoallelic state, 17.6% in , and 11.8% each in and in a biallelic state. Some mutations previously identified in pseudoachondroplasia, an allelic disorder of MED1, were shown in our study to exhibit a typical MED1 or intermediate phenotype. In contrast, it was confirmed that certain mutations in lead to MED4 phenotype. Furthermore, it has been observed that biallelic variants in may be associated with the MED5 phenotype. In patients with MED2 and MED3, the knee joint is affected, while in other types, the hip joint is predominantly affected. In 15 children followed until ages 11-18, height decreased slightly as they grew older but remained normal or at the lower limit, and slow progression was observed in the waddling gait and joint pain, except in the intermediate form. This study reveals the frequency of disease-related variants, including seven novel ones, in genes leading to MED1-5 and 7 phenotypes, and expands the spectrum of genetic and clinical phenotypes. - Source: PubMed
Publication date: 2026/04/15
Taner Hasan EmirUludağ Alkaya DilekKalyoncu Uçar AyşeŞeker AliCentel TuncayYıldırım TimurGüneş NilayTüysüz Beyhan