RUNX2 Mouse Monoclonal Antibody
- Known as:
- RUNX2 Mouse Monoclonal Antibody
- Catalog number:
- APO-000860-M04
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- RUNX2 Mouse Monoclonal Antibody
Related genes to: RUNX2 Mouse Monoclonal Antibody
- Gene:
- RUNX2 NIH gene
- Name:
- RUNX family transcription factor 2
- Previous symbol:
- CCD, CBFA1, CCD1
- Synonyms:
- AML3, PEBP2A1, PEBP2aA1
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-02
- Date modifiied:
- 2019-04-04
Related products to: RUNX2 Mouse Monoclonal Antibody
Related articles to: RUNX2 Mouse Monoclonal Antibody
- Perfluorooctanoic acid (PFOA), a persistent perfluoroalkyl substance (PFAS), has been implicated in bone mineral density loss and defective osteogenesis. In this study, by employing human fetal osteoblast (hFOB1.19), we investigated whether PFOA interferes with osteoblast differentiation by altering the transcription of genes involved in osteogenesis, and protein levels of oxidative stress defense and cannabinoid receptors (CBs). The hFOB 1.19 were exposed to increasing PFOA concentrations (1-100 µM) for seven days, representing supra-environmental concentration commonly used in mechanistic in vitro studies. Osteogenic markers were then evaluated at transcriptional level together with matrix deposition, and the results were compared to an untreated control group. Exposure to PFOA at 10 µM increased the expression of osteocalcin (BGLAP) encoding for a protein involved in calcium deposition. Catalase (CAT) protein levels were upregulated at 1 µM PFOA, while superoxide dismutase (SOD1) did not change, suggesting a selective antioxidant response to oxidative perturbation. Notably, this increase in CAT correlated with a trend toward RUNX2 upregulation, possibly representing a compensatory mechanism to preserve differentiation under oxidative stress. In addition, the highest concentration of PFOA modulated the endocannabinoid system (ECS), reducing CB1 and CB2 protein levels. Despite these molecular changes, Alizarin Red staining revealed a borderline and not statistically significant enhanced calcium deposition only at 50 µM PFOA, suggesting potentially aberrant mineralization. Overall, our findings suggest that PFOA perturbs osteoblast differentiation through oxidative stress-linked mechanisms and CBs modulation, with catalase emerging as a key protective mediator of osteogenic competence under environmental contaminants. Furthermore, the observed dysregulation of CB1 and CB2 receptors indicates that the ECS itself may represent a direct target of PFOA action in osteoblasts. - Source: PubMed
Publication date: 2026/04/15
Sella FiorenzaGiommi ChristianCarbonari DamianoLombó MartaCarnevali Oliana - Cleidocranial dysplasia (CCD) is a rare RUNX2-related skeletal disorder characterized by craniofacial anomalies and skeletal Class III malocclusion. However, the relationship between RUNX2 variant type and phenotype severity remains unclear. This study aimed to evaluate the association between RUNX2 variant types and the severity of skeletal Class III malocclusion and dental anomalies in CCD. - Source: PubMed
Chantarawaratit Pintu-OnThaweesapphithak SermpornPittayapat PishaPorntaveetus Thantrira - Glucocorticoid-induced osteoporosis (GIOP) is characterized by impaired osteoblast function and disrupted bone homeostasis during prolonged glucocorticoid exposure. This study investigated whether stem-derived extracellular vesicle-like particles (SS-EVLP) could attenuate glucocorticoid-induced osteogenic impairment and explored the potential involvement of NRF2/HO-1 signaling. - Source: PubMed
Publication date: 2026/04/11
Chen GuangmouLi HongqiangChen RihaoYao YuanLian GuanBai LipingChen HaosenZhang ChongChen Guanghua - Lung fibroblasts are key regulators of tissue homeostasis and extracellular matrix (ECM) remodeling, and their aberrant activation drives the progressive parenchymal scarring characteristic of idiopathic pulmonary fibrosis (IPF), a fatal disease with limited therapeutic options. Despite their central pathogenic role, lung fibroblasts are difficult to isolate due to their embedded position within the ECM, and standard in vitro culture conditions may lead to the loss of their native functional and transcriptional characteristics, hampering the study of fibroblast behavior in disease. The transcriptional heterogeneity of lung fibroblast subtypes and the extent to which culture-induced alterations diverge from native tissue signatures remain poorly understood. Here, we integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics of lung tissue from IPF patients and age-matched healthy donors with transcriptomic profiling of cultured fibroblasts collected at passages 1 and 6 after isolation using three optimized protocols: whole lung cell suspension (WLCS), negative fraction enrichment, and outgrowth. Tissue-based analysis identified six transcriptionally distinct mesenchymal subtypes: alveolar, adventitial, inflammatory, peribronchial, CTHRC1+ and smooth muscle cell (SMC). The fibroblast subtype CTHRC1+ represented the most transcriptionally activated pro-fibrotic subtype, showing the greatest upregulation of ECM biosynthesis genes, a prominent role in intercellular communication, and preferential enrichment within fibroblastic foci in IPF lung tissue. Pseudotime trajectory analysis supported a directional transcriptional continuum from alveolar and inflammatory fibroblasts toward the CTHRC1+ state, driven by coordinated activation of pro-fibrotic transcription factors, including RUNX2, CREB3L1, and SCX. In vitro culture progressively reshaped fibroblast transcriptional identity relative to native tissue, with increased collagen and matrix metalloproteinase (MMP) expression during passaging, loss of distinct CTHRC1+ fibroblasts, and gain of alveolar fibroblasts displaying pro-fibrotic activation across all isolation protocols. These findings provide a high-resolution transcriptional map of lung fibroblast heterogeneity in IPF and highlight critical limitations of standard in vitro culture systems for recapitulating native fibroblast diversity, with important implications for the development and evaluation of fibroblast-targeted therapeutic strategies in IPF. - Source: PubMed
Publication date: 2026/04/10
Vanegas-Avendano N DChen HWellmerling JRodriguez-Lopez JGhobashi APeters VSen CReader B FShilo KGomperts BMa QMora A LTschumperlin D JRojas M - Senile osteoporosis is characterized by a progressive decline in bone formation. Our study identifies Zfp462/ZNF462 as a novel regulator of osteoblast differentiation, providing new mechanistic insights into the aging-related change in bone formation. Here, we demonstrate that ZNF462, MOZ, and RUNX2 physically interact with each other and promote osteoblastic bone formation by increasing RUNX2 activity and histone H3 acetylation. Importantly, we reveal that aging decreases ZNF462 expression in bone cells, a process linked to reduced occupancy of the histone variant H2A.Z at the ZNF462 locus, leading to lower transcriptional activator histone H3K4 trimethylation. The osteoblast-specific Zfp462 deficiency in mice results in decreased bone mass and strength, primarily due to impaired osteoblast function. By uncovering a previously unknown ZNF462-MOZ-RUNX2 axis, this work provides a molecular basis for understanding the development of senile osteoporosis. Thus, targeting ZNF462 or MOZ could offer a new strategy to restore bone formation in aging populations. - Source: PubMed
Kim Jin-ManKim Ho KyoungMoon Sung-AhKim YewonLee Seung-HoonYu JiyoungLee Seung HunSon Woo ChanKim Jung-EunBaek In-JeoungKim Young-BumKoh Jung-Min