RUNX2 antibody - middle region (ARP36679_T100)
- Known as:
- RUNX2 (anti-) - middle region (ARP36679_T100)
- Catalog number:
- arp36679_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RUNX2 antibody - middle region (ARP36679_T100)
Related genes to: RUNX2 antibody - middle region (ARP36679_T100)
- 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 antibody - middle region (ARP36679_T100)
Related articles to: RUNX2 antibody - middle region (ARP36679_T100)
- Orthodontically induced inflammatory root resorption (OIIRR) is a common complication associated with excessive compressive force during orthodontic treatment, leading to irreversible cementum destruction. However, the cellular and molecular mechanisms underlying this process remain unclear. This study aimed to investigate the role of the mechanosensitive ion channel Piezo1 in regulating cementoblast function under mechanical stress. Cementoblasts (OCCM-30) were subjected to 1 g/cm of compressive force, and global gene expression was analyzed via RNA sequencing, revealing 6932 differentially expressed genes. Compressive force upregulated the expression of HIF-1α and its downstream angiogenesis-related genes (Vegf, Angpt1, Angptl4), while significantly downregulating osteogenic markers such as RUNX2 and SP7, leading to suppressed mineralization and calcium nodule formation. Activation of Piezo1 using the agonist Yoda1 mimicked the effects of compressive force, whereas inhibition by GSMTX4 reversed them. Interestingly, depletion of extracellular calcium did not affect these outcomes, suggesting that Piezo1 acts independently of calcium influx in this context. Moreover, Piezo1 activation and compressive force co-upregulated LIM and cysteine-rich domains 1 (LMCD1) and downregulated Periostin (POSTN), both of which were identified as novel downstream effectors of Piezo1 signaling. These changes were also reversed by Piezo1 inhibition. In conclusion, compressive force impairs cementoblast mineralization while enhancing hypoxia and angiogenic pathways through Piezo1 activation. LMCD1 and POSTN may serve as new molecular targets for understanding and potentially preventing OIIRR. This study provides important insights into the mechanotransduction mechanisms in cementoblasts and identifies Piezo1 as a key regulator linking mechanical stimuli to pathological root resorption. - Source: PubMed
Publication date: 2026/06/09
Wang YaoWang LeiRuf SabineStaszyk CarstenGroeger Sabine - YAP/TAZ signaling is required for initiation of lung alveolar repair, yet previous studies in idiopathic pulmonary fibrosis (IPF) predicted increased YAP/TAZ signaling in alveolar epithelial cells (AECs). We investigated whether persistent YAP/TAZ AEC signaling contributes to failed epithelial repair and persistent fibrotic remodeling. In IPF lungs, we identified increased YAP+/TAZ+ AECs and increased transcriptional target expression. Pharmacological YAP/TAZ activation in human AEC organoids and in murine AT2 cell organoids generated with genetic YAP/TAZ activation (YTactive) (via deletion of Hippo-kinases Stk3/4), resulted in phenotype shifts into aberrant transitional and airway-like states. Bleomycin injury of YTactive mice resulted in persistent fibrotic remodeling at 28- and 56-days post-bleomycin injury. Gene promoter activity associated with transitional cell markers (Krt19, Hopx, and Runx2) was increased in YTactive AT2 cells. Immunofluorescent staining showed a loss of AT2 associated Cebpa and increased Krt19 in YTactive lineage traced AT2 cells 28 days post-injury. Inhibition of YAP/TAZ using Verteporfin resulted in improved lung repair in YTactive mouse lungs, including restored Cebpa and decreased Krt19+ transitional cells. These findings demonstrate sustained YAP/TAZ activation drives abnormal alveolar repair and persistent fibrotic remodeling. Blocking aberrant persistent YAP/TAZ activity promotes adaptive repair and has potential as a therapeutic strategy for pulmonary fibrosis. - Source: PubMed
Publication date: 2026/06/09
Gaona Isabella PMcCall A ScottGeis Natalie MColvard Arlo CDiGiovanni Gianluca TSherrill Taylor PSingha Ujjal KNichols David SSerezani Ana PDavid Holly ECartailler Jean-PhilippeShrestha ShristiGutor Sergey SBlackwell Timothy SKropski Jonathan AGokey Jason J - The development of 3D-scaffolds to treat critical-size bone defects in orthopedic and reconstructive surgery remains a challenge due to low oxygen diffusion causing cell death in the core of the scaffolds. Perfusion cell culture and fluid-conducting hollow channels might be critically important to enhance oxygen diffusion. Therefore, we aimed to test whether perfusion cell culture synergistically improves oxygen diffusion and osteogenic activity in multi-channeled 3D-porous silk fibroin scaffolds with pre-osteoblasts using experiments and finite element modeling. - Source: PubMed
Publication date: 2026/06/09
Seddiqi HadiSaatchi AlirezaYekani FarshidYahyazadeh AminJin JianfengAmoabediny GhassemZandieh-Doulabi BehrouzKlein-Nulend Jenneke - Tuberculosis (TB) remains a global health threat, affecting over a million children under the age of 15 annually. Many children with TB do not receive treatment due to challenges in diagnosis. - Source: PubMed
Publication date: 2026/06/08
Mousavian ZaynabSegal Mark RCalderon Roger ILuiz JuanetaNkereuwem EsinWambi PeterParadkar MandarFranke Molly FKällenius GunillaKampmann BeateKinikar AartiSigal George BSundling ChristopherSwaney Danielle LWobudeya EricZar Heather JCollins Jeffrey MCattamanchi AdithyaErnst Joel DJaganath Devan - Cellular communication network (CCN) proteins are key matricellular regulators of cartilage development, yet their species-specific roles and network-level context remain unclear. This study integrated bulk RNA sequencing from chicken and mouse embryonic limb bud micromass cultures and human mesenchymal stem cell chondrogenesis with co-expression, protein-protein interaction, and ortholog analyses to construct CCN-centered regulatory networks across models. CCN1 and CCN2 emerged as dominant, conserved hubs enriched in collagen-containing extracellular matrix, cartilage development, and growth factor signaling modules, whereas CCN3-CCN6 showed lower context-dependent expression and connectivity. Functional and ortholog analyses revealed moderate pathway conservation, with high conservation of IGF, EGFR, and HIF-1 signaling, but reduced overlap in hypoxia and mechanosensing/Hippo categories, indicating species-specific tuning of environmental sensing. A focused ortholog screen identified multifunctional conserved hubs, including , , , , , , , and . Single-cell RNA-seq meta-analysis of human iPSC-derived chondrogenesis and embryonic limb datasets showed CCN1/2 expression and homologous network activity peaking in mesenchymal and early chondrocyte populations, consistent with model-dependent persistence into hypertrophic and ossification stages in vivo. Overall, this work defines a conserved CCN1/2-centered axis integrating extracellular matrix formation with growth factor and mechanical cues, providing a framework for model selection and CCN-targeted cartilage regeneration strategies. - Source: PubMed
Publication date: 2026/06/02
Wang ZhangzhengVágó JuditTakács RolandPóliska SzilárdKim Ee HyunJin Eun-JungKubota SatoshiKleer Celina GPerbal BernardMatta Csaba