RUNX3 Monoclonal Antibody [R31E10]
- Known as:
- RUNX3 Monoclonal Antibody [R31E10]
- Catalog number:
- A-0514-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- RUNX3 Monoclonal Antibody [R31E10]
Related genes to: RUNX3 Monoclonal Antibody [R31E10]
- Gene:
- RUNX3 NIH gene
- Name:
- RUNX family transcription factor 3
- Previous symbol:
- CBFA3
- Synonyms:
- AML2, PEBP2A3
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-02
- Date modifiied:
- 2019-04-04
Related products to: RUNX3 Monoclonal Antibody [R31E10]
Related articles to: RUNX3 Monoclonal Antibody [R31E10]
- The relationships among obesity, accelerated biological aging, and asthma, as well as the underlying epigenetic mechanisms, remain incompletely understood. - Source: PubMed
Publication date: 2026/05/21
Liu JianSong ZhengqiShi ChenggeLu XinanZhang AijunChen YiheZhang Xuejia - Exosomes are endogenous vesicles that transport microRNAs (miRNAs), thereby mediating intercellular communication. This study was assigned to expound the regulatory role of exosomal miR-147-3p in asthma progression. The ovalbumin-mediated murine model of asthma was established to obtain bronchoalveolar lavage fluid (BALF), and exosomes were isolated by ultrafiltration centrifugation. Differential expression of exosomal miRNA and mRNA was analyzed by RT-PCR. Dual-luciferase was utilized to validate potential binding between key miRNAs and target genes. Additionally, the impact of miRNA mimics and BALF-exosomes on growth of bronchial epithelial cells (BECs) was assessed, followed by RT-qPCR and Western blot. Ovalbumin exposure induced asthma phenotypes in mice. Notably, miR-147-3p and miR-146b-5p were markedly elevated in BALF exosomes from asthmatic mice, whereas miR-98-5p and RUNX3 were markedly decreased. Luciferase assay confirmed the direct binding of miR-147-3p to RUNX3 mRNA 3' UTR. Furthermore, PKH26-labeled exosomes were internalized by BECs. Asthmatic BALF-exosomes or miR-147-3p mimics reduced cell viability and migration while promoting apoptosis. This phenomenon could be reversed by miR-147-3p inhibition. miR-147-3p overexpression or asthmatic BAF-exosomes suppressed RUNX3 protein and mRNA expression. BALF-derived exosomal miR-147-3p modulated behaviors of BECs via targeting RUNX3, suggesting its potential as a therapeutic target and biomarker for asthma pathogenesis. - Source: PubMed
Huang XunZuo QiYuan YuyunHuang SihongZhang YantaoShen Yiyun - Chronic non-bacterial osteomyelitis (CNO) is a rare autoinflammatory bone disease primarily affecting children and adolescents. Reliable biomarkers for diagnosis, disease monitoring, and prediction of disease course are lacking. This study demonstrates that, when compared to healthy participants, the proportion of 'pro-inflammatory' CD14CD16 'classical' monocytes is elevated in patients with CNO, before and after the initiation of treatment. Differential DNA methylation (200 hyper-, 162 hypo-methylated) profiles in monocytes from CNO patients affect key genes involved in immune regulation, including RUNX3, HOXA9, HLA-DMB, HLAB, MAP3K6, RXRB, CD163L1, MAP2, CDK6, HLA-G, HDAC10, and HLA-DQA1 genes. Notably, DNA methylation changes persist and potentially progress over time after the initiation of treatment with naproxen. In conclusion, patients with CNO display higher proportions of 'classical' monocytes when compared to healthy participants in conjunction with dysregulated DNA methylation patterns. Molecular alterations remain despite symptom relief with naproxen, suggesting progressive inflammation-mediated changes. - Source: PubMed
Publication date: 2026/05/15
Carlsson EmilGodoy-Tena GerardMorbach HennerGirschick Hermann JDissanayake DilanCharras AmandineBallestar EstebanHedrich Christian M - Microsatellite-stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, with limited CD8⁺ T cell infiltration and poor responsiveness to immune checkpoint inhibitors (ICIs). Here, using an in vivo CRISPR/Cas9 screen in a CMT93 cell-derived murine tumor model, we identify Arid3b as a key negative regulator of CD8⁺ T cell infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhances their intratumoral accumulation and promotes robust tumor control. Mechanistically, Arid3b deficiency upregulates Runx3, driving a tissue-resident memory-like phenotype and effector function. Notably, the benefits conferred by Arid3b deficiency are abrogated upon Runx3 deletion, indicating a RUNX3-dependent mechanism. Together, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy. - Source: PubMed
Publication date: 2026/05/15
Wang ShuoHou SenLuo CeZhang HaoruiJin YitengZhang RuiZhao YanpingXiong XiaoyuGuo RuiWang ChaoBao YudiWen LiangPan DengYe YingjiangZeng ZexianGao Zhidong - The transcription factor Runx3 modulates key gene expression programs important for the development of multiple tissues. Here, we uncover new functions for Runx3 in thymic epithelial lineage development and show Runx3 expression in medullary thymic epithelial cells (mTECs) is required for both Autoimmune Regulator + (Aire) mTEC development and tissue-specific antigen (TSA) gene expression. Consequently, TEC-specific deletion of Runx3 in mice results in a profound decrease in Aire mTECs, a global loss of TSA gene expression, and the development of autoimmunity. Moreover, loss of Runx3 in TECs results in an expansion of immature CCL21 mTECs and a loss of Aire-dependent mimetic cells. Single-cell analysis reveals Runx3 modulates core transcriptional programs in TECs that correlate with the observed cellular changes. Our findings highlight a previously undescribed role for Runx3 in mTEC development and thymic central tolerance. - Source: PubMed
Publication date: 2026/05/15
Sin Jun HyungPhillips Sloan HParent Audrey VWaterfield Michael R