SOX9 antibody Host Rabbit
- Known as:
- SOX9 (anti-) Host Rabbit
- Catalog number:
- 'H00006662-D01P
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9 antibody Host Rabbit
Related genes to: SOX9 antibody Host Rabbit
- 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 Host Rabbit
Related articles to: SOX9 antibody Host Rabbit
- 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 - The complex microenvironment of articular cartilage defects, characterized by oxidative stress and infection risk, poses a major challenge for regenerative medicine. Here we report a molecular engineering strategy to transform mung bean protein (MBP), an abundant and sustainable plant protein, into a multifunctional, microenvironment-relevant bioink. By sequentially grafting ε-polylysine (EPL) and methacryloyl groups onto the MBP backbone, we created a family of photocurable derivatives (MEM) with tunable methacrylation degrees. Three variants were obtained: MEM-A (65% methacrylation), MEM-B (78% methacrylation), and MEM-C (86% methacrylation). The hydrogels exhibit rapid rheological gelation (<2 s, defined by the '-″ crossover), tunable mechanical properties (20-60 kPa compressive modulus), and a porous architecture (100-150 μm pore size, 70-80% porosity) conducive to cell growth. The resulting MEM hydrogels integrate broad-spectrum antimicrobial activity (>90% bacterial killing), enhanced antioxidant capacity (>51% radical scavenging), and excellent DLP printability (>87% printing accuracy). Among these, the MEM-B hydrogel supports chondrocyte viability, upregulates cartilage-specific genes (), and downregulates oxidative stress markers (). In a rat osteochondral defect model, MEM-B promoted robust cartilage regeneration with superior ICRS scores and tissue integration compared to GelMA controls. This work establishes a design paradigm for converting underutilized plant proteins into multifunctional bioinks that actively engage with pathological microenvironments, opening sustainable avenues for next-generation regenerative biomaterials. - Source: PubMed
Publication date: 2026/06/13
He XiaoliZhou ZhengZhu ShuaiChen XinYan ShipingYang LingxiuLei JiajieDai YaoLiu Hairong - Astrocytes play essential roles in neuronal development, function, and disease, yet existing methods to derive astrocytes from human pluripotent stem cells (hPSCs) are complex and can involve months of maturation. We developed a genomic safe-harbor knock-in system for inducible expression of the astrogenic transcription factors NFIA, NFIB, and SOX9, enabling rapid and robust generation of functional induced astrocytes (iAstrocytes). Across five hPSC lines, NFIB-SOX9 and NFIA-NFIB-SOX9 combinations efficiently generated highly pure populations expressing astrocyte-specific and synaptogenic genes. iAstrocytes displayed cytokine-induced expression of complement factors C3 and C4 and were amenable to CRISPR interference (CRISPRi) gene expression knockdown. Optimization of culture conditions enabled survival of NFIB-SOX9 iAstrocytes in co-culture with human induced neurons (iNeurons). Through pharmacological and genetic perturbations, we uncovered a previously undescribed phenomenon in which co-culture with iAstrocytes promoted the development of synchronized iNeuron network calcium activity mediated by specific gap junction proteins. This rapid and genetically tractable iAstrocyte platform provides a robust model to dissect human genetic and environmental effects on astrocyte-neuron interactions. - Source: PubMed
Publication date: 2026/06/05
Morshed NaderDemers MatthewGonzalez-Ramos AnaJäntti HennaDoman JordanD'Souza SeanLi LetianGranger Adam JJohnson Matthew BStevens Beth