MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Known as:
- MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Catalog number:
- arp32018_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MEOX1 Antibody - C-terminal region (ARP32018_P050)
Related genes to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Gene:
- MEOX1 NIH gene
- Name:
- mesenchyme homeobox 1
- Previous symbol:
- -
- Synonyms:
- MOX1
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-14
- Date modifiied:
- 2016-11-09
Related products to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
Related articles to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
- The intricate interactions between environmental exposures, the respiratory microbiome, and host genetic variations remain inadequately understood in the context of respiratory health. This study utilized sputum metagenomic data from 1,651 individuals in our previous cohort to elucidate these associations. Mendelian randomization indicated that air pollutants (e.g., SO, CO, and PM) were associated with lung function, which is potentially mediated by microbes, such as , , and spp. Several genetic loci associated with respiratory microbiome variation were found to be linked to genotype-dependent associations between environmental exposures and lung function. For bacteria, the locus (rs1973191819) was associated with lower abundance under air pollutant exposure. The (1:26157175) and (rs1343834070) loci showed associations with higher levels of certain pathogenic taxa (e.g., , ) and lower levels of the commensal , increasing chronic obstructive pulmonary disease (COPD) risk. For fungi, and loci exhibited associations with and abundance, respectively. These genotype-dependent associations between the microbiome and environmental exposures provide insights into airway dysbiosis and susceptibility to respiratory diseases. - Source: PubMed
Publication date: 2026/07/29
Xu ShifenYang LeiGao JingyuanShi YunfengTang XinCai HanqinYang LilingHan YuanyuanLin LifengMeng RuilinSun JiufengGuan Wei-JieTang TaoShu WenshengCao ChaoZheng Xue-YanWang ZhangYi Xinzhu - Osteoporosis is a highly heritable metabolic bone disorder characterized by low bone mass and increased fracture risk. However, the causal genes underlying disease susceptibility remain incompletely understood. In this study, we employed a summary-data-based Mendelian randomization (SMR) framework to identify genes with potential causal effects on osteoporosis by integrating genome-wide association study summary statistics from the FinnGen consortium with multilayer molecular quantitative trait loci (xQTL) data, including expression, splicing, methylation, and protein QTLs across multiple tissues (106 xQTL datasets in total). The heterogeneity in dependent instruments (HEIDI) test was applied to distinguish pleiotropic associations from linkage disequilibrium-driven effects. Functional characterization was further conducted using Gene Ontology and KEGG pathway enrichment analyses, protein-protein interaction network construction, drug-gene enrichment analysis, and molecular docking. Using this integrative approach, we identified 15 high-confidence genes - CEP112, CKB, GID4, MEOX1, MEPE, PPP6R3, RGS9, RSPO3, SERPINA1, SFRP4, SOST, SPP1, SREBF1, TOM1L2, and ZBTB48 - showing evidence of causal associations with osteoporosis after stringent multiple-testing correction and HEIDI filtering. These genes included established regulators of bone metabolism as well as novel candidates involved in metabolic regulation and signal transduction. Enrichment analyses highlighted pathways related to Wnt and bone morphogenetic protein signaling, extracellular matrix organization, and metabolic processes, while network analysis revealed substantial functional connectivity among the prioritized genes. In addition, drug-gene enrichment analysis prioritized β-carotene, apocarotenal, and bezafibrate as potential therapeutic candidates, with molecular docking supporting stable interactions with key protein targets. Overall, this study provides robust genetic evidence for causal molecular regulators of osteoporosis and highlights potential therapeutic targets, offering a clinically relevant resource for future functional validation and translational research. - Source: PubMed
Yu FeiWan XiwenQiu Jiaxuan - Salivary adenoid cystic carcinoma (SACC) is a malignant salivary gland neoplasm characterized by aggressive local invasion and a marked propensity for metastasis. However, the role of MEOX1 in SACC progression remains poorly defined. In this study, we examined the effects of MEOX1 overexpression on the malignant behavior of SACC cells in vitro and in vivo. Human SACC-83 and SACC-LM cells were transduced with lentiviral vectors encoding MEOX1 or an empty vector control, and cell proliferation, migration, invasion, and cell cycle distribution were assessed using CCK-8, wound healing, Transwell, and flow cytometric assays, respectively. RNA sequencing was performed to characterize transcriptional changes associated with MEOX1 overexpression. In vivo, tumor growth was evaluated in BALB/c nude mice bearing subcutaneous xenografts, and pulmonary metastatic colonization was assessed using a tail vein injection model. MEOX1 overexpression reduced the proliferation, migration, and invasion of SACC cells in vitro and increased the G2/M phase fraction. In xenograft models, MEOX1-overexpressing cells formed smaller tumors and showed lower Ki67 staining than control cells. In the experimental lung metastasis model, mice injected with MEOX1-overexpressing cells developed fewer pulmonary metastatic nodules. RNA-seq identified 588 differentially expressed genes associated with MEOX1 overexpression, with enrichment in pathways including cytokine-cytokine receptor interaction, Toll-like receptor signaling, and G protein-coupled receptor signaling. Together, these findings indicate that enforced MEOX1 expression is associated with reduced malignant phenotypes in SACC models and with transcriptomic alterations in pathways related to immune response, G protein-coupled receptor signaling, and DNA damage response. - Source: PubMed
Publication date: 2026/05/06
Sun HuaxiuLiu YupingCui YajuanZhou ZhengWu ZhanlanZhou Chuan-Xiang - Mesenchyme homeobox 1 (MEOX1) has been characterised as a central transcriptional regulator of fibroblast activation. Ligustilide (LIG) has significant antifibrotic, anti-inflammatory and antioxidative activities. We investigated if LIG can ameliorate hepatic fibrosis by targeting MEOX1 and exploring the underlying mechanism. - Source: PubMed
Publication date: 2026/05/12
Luan QinrongWang ZhechengWang YueXu JialiWang GuorongHu ZhehaoZhou JunjunTian XiaofengZhao YanYao Jihong - Lymph node metastasis (LNM) is a pivotal determinant of poor prognosis in ovarian cancer (OC), yet how tumor-intrinsic programs remodel the microenvironment to enable spread remains unclear.Here, we identify the transcription factor mesenchymal homeobox 1 (MEOX1) as an upstream coordinator, whose overexpression associates with LNM, increased lymphatic density, and poor survival based on integrative analyses of public datasets and our 113-patient cohort. In an in vivo LNM model, MEOX1 overexpression enhances tumor burden, lymphatic vessel density, and LNM, whereas tumor-conditioned medium does not directly activate lymphatic endothelial cells (LECs), implicating stromal intermediates. Spatial transcriptomic and immunostaining analyses confirmed cancer-associated fibroblast (CAF)-LEC proximity and vascular endothelial growth factor-C (VEGF-C) localization within CAFs, supporting a CAF-dependent lymphangiogenic route. Mechanistically, MEOX1 binds the sphingosine kinase 1 (SPHK1) promoter to activate sphingosine-1-phosphate (S1P) synthesis, driving a dual autocrine-paracrine program: sphingosine-1-phosphate receptor 3 (S1PR3)-dependent signaling promotes tumor proliferation/migration, while S1P/S1PR1 reprograms fibroblasts into VEGF-C-secreting, alpha-smooth muscle actin (α-SMA)-positive CAFs that stimulate lymphangiogenesis and LNM; SPHK1 inhibition blunts these phenotypes, whereas S1P supplementation restores them. These findings provide novel insights into lymphatic metastasis and demonstrate that metastatic competence depends not only on intrinsic tumor aggressiveness but also on the acquired ability to construct a pro-dissemination niche. - Source: PubMed
Publication date: 2026/05/10
Li JiajiaZhi XiulingLin QianhanSun YatingSun YihuaAbudousalamu ZulimireXue MengyangZheng ChangLi XiaotianYao LiangqingChen Mo