SOX9 Antibody (Center) Blocking Peptide
- Known as:
- SOX9 Antibody (Center) Blocking Peptide
- Catalog number:
- BP1409c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SOX9 Antibody (Center) Blocking Peptide
Related genes to: SOX9 Antibody (Center) Blocking Peptide
- Gene:
- SOX9 NIH gene
- Name:
- SRY-box 9
- Previous symbol:
- CMD1, CMPD1
- Synonyms:
- SRA1
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-25
- Date modifiied:
- 2018-06-25
Related products to: SOX9 Antibody (Center) Blocking Peptide
Related articles to: SOX9 Antibody (Center) Blocking Peptide
- Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine skin cancer with a poorly understood cell of origin and initiation process. Most MCC tumors feature monoclonal integration of Merkel cell polyomavirus (MCPyV) DNA, which expresses viral small T (sT-Ag) and large T antigens (LT-Ag), responsible for driving MCC tumors. The process by which MCPyV T antigens (T-Ags) transform cells to initiate MCC has been unclear, in part due to the lack of physiologically relevant in vivo models. Building upon our previous work, which demonstrated that SOX9-expressing (SOX9+) hair follicle Merkel cell progenitors are susceptible to T-Ag-mediated reprogramming, we establish a mouse model in which sT-Ag expression and Trp53 attenuation in SOX9 cells produce metastatic neuroendocrine tumors with histopathologic and immunophenotypic features of human MCC. Importantly, while sT-Ag alone induces partial MCC-associated gene expression, suppression of p53 is required for sT-Ag to induce neuroendocrine lineage transdifferentiation in the hair follicle. Cumulatively, these studies enhance our knowledge of MCC biology and establish a de novo MCC tumorigenesis model in a tractable immunocompetent system that will be invaluable for further advancements in the field. - Source: PubMed
Publication date: 2026/06/16
Weber MadisonAckermann AmandaLi Meng-YenMeehan Shane AEzhkova Elena - Osteochondral defects require the simultaneous regeneration of cartilage and subchondral bone, posing a major challenge for current biomaterial strategies. Here, we present a radially oriented 3D-printed bilayer hydrogel scaffold composed of a mechanically reinforced GelMA/HAP osteogenic layer and a compliant, KGN@Lip-loaded GelMA chondrogenic layer, to achieve coordinated osteochondral repair. Structural and physicochemical characterization confirmed the formation of a functionally graded architecture with uniform HAP and KGN@Lip distribution, while mechanical, rheological, swelling, and degradation analyses revealed a layer-dependent gradient that resembles certain structural features of the native osteochondral interface. , the GelMA/HAP layer promoted robust osteogenic differentiation through ion-mediated activation of osteogenic pathways, whereas the GelMA/KGN@Lip layer sustained chondrogenic stimulation and markedly enhanced SOX9, Col2a1, and Acan expression. The radially oriented microchannels provided an interconnected structure that may support nutrient transport and cell infiltration. implantation demonstrated substantial subchondral bone regeneration and the formation of cartilage-like tissue with improved matrix organization, along with enhanced integration at the osteochondral interface, confirming the scaffold's ability to provide spatially coordinated biochemical and structural cues. Overall, this anisotropic bilayer hydrogel scaffold offers a promising strategy for integrated and functional osteochondral regeneration. - Source: PubMed
Publication date: 2026/06/12
Wangzi ZhenbiaoYang ChengchengYu PengHuang XiubiaoHu NanJiao TuoQi Hao - Synovial sarcoma is a translocation-associated soft-tissue sarcoma defined by the SS18-SSX fusion gene and typically exhibits biphasic or monophasic histology with at least focal epithelial marker expression. However, rare cases with diffuse myxoid stroma may closely mimic other myxoid sarcomas, which can pose a diagnostic challenge. A 61-year-old woman presented with a gradually enlarging mass on the posterior aspect of the right thigh. Magnetic resonance imaging revealed a 55-mm soft tissue tumor with heterogeneous high signal intensity on T2-weighted images and partial contrast enhancement. Core needle biopsy demonstrated atypical spindle to round cells within a prominent myxoid background. Immunohistochemically, cytokeratin was negative and SOX9 was diffusely positive, raising suspicion for extraskeletal myxoid chondrosarcoma. The patient underwent marginal excision followed by postoperative radiotherapy; however, lung metastasis and local recurrence subsequently developed. Comprehensive genomic profiling identified an SS18-SSX1 fusion gene, and the diagnosis of synovial sarcoma was confirmed by fluorescence hybridization and reverse transcription polymerase chain reaction in both the primary and recurrent tumors. RNA sequencing further verified the SS18-SSX1 fusion and demonstrated no additional pathogenic or clinically relevant fusion transcripts. Histologically, the tumor consistently exhibited a diffuse myxoid stroma with a focal reticular pattern, closely resembling extraskeletal myxoid chondrosarcoma. It lacked epithelial marker expression, including cytokeratin and epithelial membrane antigen (EMA), throughout the disease course. To our knowledge, this case represents a rare presentation of synovial sarcoma arising in the extremity with diffuse myxoid stroma and complete absence of epithelial marker expression, with the diagnosis confirmed by molecular identification of the specific fusion transcript. This case highlights that synovial sarcoma can exhibit a myxoid phenotype and may lack epithelial marker expression, both of which can complicate the diagnosis. It also underscores the importance of integrating molecular analyses, particularly fusion-oriented genomic testing, for accurate diagnosis in challenging soft-tissue tumors. - Source: PubMed
Publication date: 2026/05/29
Miyazaki TomohiroOike NaokiAriizumi TakashiMurayama YudaiOgose AkiraSugino HideakiNakamura MaiKondo ShuheiTani YusukeUmezu HajimeKawashima Hiroyuki - Gene therapy combined with advanced biomaterial-based delivery systems represents a powerful strategy to enhance chondrogenic differentiation of mesenchymal stem cells (MSCs), enabling the development of next-generation regenerative therapies for cartilage repair. In this context, gene-activated biomaterials provide a versatile tool for spatially and temporally regulating cell fate within three-dimensional (3D) microenvironments. Here, we combine collagen type I/type II-hyaluronic acid (CI/CII-HyA) scaffold with a novel non-viral gene delivery platform based on niosomes (DP20CQ) to deliver the master chondrogenic transcription factor SOX9 using either parental (PP) or minicircle (MC) plasmids, thereby promoting chondrogenesis in MSCs. After 28 days under chondrogenic conditions, DP20CQ-based scaffolds promoted a more favourable chondrogenic-to-hypertrophic profile than gene-free or Lipofectamine (LPF)-based scaffolds while preserving metabolic activity. Sustained SOX9 overexpression was evidenced in both PP and MC niosome-based systems at the gene and protein levels. Similarly, both systems showed an upregulation of key chondrogenic markers, including aggrecan (ACAN) and collagen type II (COLII), together with the concomitant downregulation of fibrocartilage (collagen type I, COLI) and hypertrophic (collagen type X, COLX) markers, with DP20CQ/MC exhibiting the highest expression ratios. Taken together, these findings demonstrate that DP20CQ-activated biomaterials enable efficient and sustained genetic regulation in MSCs within a 3D microenvironment, promoting the formation of hyaline-like cartilage while suppressing hypertrophic differentiation. This strategy constitutes a versatile gene-activated biomaterial platform with promising potential for cartilage regeneration. - Source: PubMed
Publication date: 2026/06/11
López-Seijas JunqueraIglesias-Fente AlbaIntini ClaudioDobricic MarkoO'Brien Fergal JRey-Rico Ana - Circular RNAs (circRNAs) are important regulators of signaling pathways involved in intervertebral disc degeneration (IVDD). This study investigated the role and underlying mechanism of circTMEM230 in the degeneration of endplate chondrocytes. We observed that circTMEM230 expression was significantly downregulated in chondrocytes subjected to intermittent cyclic mechanical tension (ICMT). Functional assays demonstrated that overexpression of circTMEM230 enhanced the expression of extracellular matrix (ECM)-related genes through modulation of the miR-223-3p/FOXO3/SOX9 signaling axis. Specifically, circTMEM230 acted as a molecular sponge for miR-223-3p, thereby upregulating FOXO3, which subsequently promoted SOX9 transcription. In vivo experiments further confirmed that circTMEM230 mitigated IVDD progression and regulated the expression of miR-223-3p, FOXO3, and SOX9. Additionally, expression levels of circTMEM230, miR-223-3p, FOXO3, and SOX9 were found to be correlated in endplate cartilage tissue samples from IVDD patients. These findings suggest that circTMEM230 exerts a protective role in IVDD and may serve as a promising therapeutic target for further investigation. - Source: PubMed
Zheng QuanYang JiongLi Xing-XingShao SongWang Chuan-DongWang Qi-WeiSun Liang-Ye