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)
- Accumulation of extracellular matrix (ECM) causes tissue fibrosis that contributes to myocardial dysfunction and heart failure (HF), yet there are no approved anti-fibrotic therapeutics that target it. Inhibitors of BET proteins (BETi) reduced fibrosis in preclinical HF models, and clinical-stage BETi, apabetalone, reduced hospitalizations for HF in a phase 3 trial, but our mechanistic understanding is incomplete. Here we tested apabetalone for anti-fibrotic activity in cell models that recapitulate cardiac fibrosis. - Source: PubMed
Publication date: 2026/09/09
Wasiak SylwiaGilham DeanFu LiTsujikawa Laura MCarestia AgostinaSarsons Christopher DTeng GuoqiTurnbull Jeannine DHassanabad Ali FatehiSweeney MichaelFedak Paul W MKulikowski Ewelina - Direct reprogramming of cardiac fibroblasts (CFs) into induced cardiomyocytes (iCMs) holds promise as a therapeutic strategy for heart regeneration. After myocardial infarction (MI), resident quiescent CFs (QCFs) activate and differentiate into myofibroblasts (MFs) in the infarcted region that drive pathological cardiac fibrosis. Converting these injury-activated MFs into iCMs could simultaneously alleviate fibrosis and replenish lost cardiomyocytes. However, whether the marked heterogeneity of CFs in the infarcted heart, and in particular the activation of QCFs into MFs, creates an intrinsic barrier that limits the reprogramming of these injury-activated MFs remains unknown. - Source: PubMed
Publication date: 2026/09/08
Wu JingdongYang ChunyanWu DonghuiZhu ShaoqiLiu YiranYang YangXu ZeXu YitongYang XiaochunMao LichaoChen JinxuanWang HuanZhao DongyuWang ShiqiangTang ChaoZhou BinZhao Yang - Fibroblasts adopt diverse cell states in response to inductive cues to maintain tissue homeostasis. We leveraged this cell-state plasticity to define how genome organization contributes to changes in cellular identity. We show that TGF-β reconfigures topologically associating domains and chromatin loops at genes upregulated during fibroblast activation into myofibroblasts. Cohesin is required for gene induction during fibroblast activation, and enhanced cohesin stability is sufficient to bypass TGF-β signaling and drive a myofibroblast-like state. Emerging evidence suggests chromatin spatial positioning relative to nuclear speckles can regulate gene expression. Therefore, we examined the role of the critical nuclear speckle component SON and showed that it is required for myofibroblast gene expression. Notably, enhancing genome folding partially rescued gene expression in fibroblasts with SON-depleted nuclear speckles. Together, these findings advance our understanding of fibrosis and support a model in which distinct facets of genome organization converge to orchestrate cell-state transitions. - Source: PubMed
Publication date: 2026/08/14
Gardner ZacharyLinares-Saldana RicardoHaridhasapavalan Krishna KumarMéndez Fernández Pedro OBarka VasiaYang RachelKoch-Bojalad BaileyPadmanabhan ArunWang QiaohongShah Parisha PNguyen Son CJoyce Eric FJain Rajan - 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