MATN3 Antibody (OAPB00875)
- Known as:
- MATN3 Antibody (OAPB00875)
- Catalog number:
- oapb00875
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MATN3 Antibody (OAPB00875)
Ask about this productRelated genes to: MATN3 Antibody (OAPB00875)
- 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 (OAPB00875)
Related articles to: MATN3 Antibody (OAPB00875)
- 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 - Jeju native pig (JNP) is an indigenous breed originating from Korea, characterized by short black hair, small stature, and superior meat quality compared with commercial breeds. This study investigated meat quality and transcriptome differences in the muscles of Landrace and JNP pigs. Phenotypic analysis of meat quality traits was performed on each breed, revealing significant differences in cooking loss, crude fat, moisture, CIE L*, CIE a*, shear force, pH, hardness, gumminess, and chewiness (p<0.05). JNP exhibited significantly higher intramuscular fat content and CIE a* (p<0.001), which increases consumer preference, suggesting that JNP have superior meat quality traits. To understand transcript expression differences, indicating differences in meat quality characteristics and growth between the two breeds, RNA sequencing was performed on muscle samples from each breed. Overall, 427 differentially expressed genes (DEG) were upregulated in JNP, while 821 genes were upregulated in Landrace. Among these, , and were key candidate genes. Enrichment analysis in Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways suggested DEG are involved in biological processes such as the cell cycle, extracellular space, collagen trimer, platelet-derived growth factor binding, and motor proteins. This study provides important insights into the genetic expression characteristics of Landrace and JNP and elucidates the mechanisms related to economic traits, such as superior meat quality and growth rate. Additionally, these findings provide foundational data for improving meat quality and suggest strategies for the genetic improvement of both breeds. - Source: PubMed
Publication date: 2025/11/01
Kim Na-YoungLee SanghoonKim Hyeon-AhKang Yong-JunCho In-CheolPark Jong-Eun - Multiple epiphyseal dysplasia (MED), caused by mutations in MATN3, is a chondrodysplasia affecting the cartilage growth plate and is characterised by delayed epiphyseal ossification, short stature, and early onset osteoarthritis. Here we generated an in vitro human pluripotent stem cell (hPSC) model of cartilage growth-plate development to identify pathogenic mechanisms underlying MED. - Source: PubMed
Publication date: 2026/02/04
Woods StevenBates NicolaCain StuartHumphreys Paul E AMancini Fabrizio EAguero Burgos BrendaHarley PeterAlqahtani Rayed Ali AKamprom WitchayaponMironov AleksandrAdamson AntonyDonaldson Ian JMortier GeertChandler KateNicolaou AnnaBaldock ClairSchwartz Jean-MarcKimber Susan J