SOX9
- Known as:
- SOX9
- Catalog number:
- ARP37986_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9
Related genes to: SOX9
- 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
Related articles to: SOX9
- BackgroundPost-traumatic ankle osteoarthritis (TAA) is driven by injury-related inflammation, cartilage matrix loss, and chondrocyte phenotypic instability. Indian hedgehog (IHH) is implicated in hypertrophic and catabolic cartilage remodeling, but whether local miR-199a-5p administration is associated with changes in IHH-related expression patterns in traumatic ankle cartilage remains incompletely defined.MethodsForty-eight male Sprague-Dawley rats were randomized to sham, TAA model, miR-199a-5p agomir, or negative-control agomir groups. TAA-like cartilage degeneration was induced by medial malleolar fracture followed by unrestricted cage activity. From week 2, rats received weekly intra-articular saline, miR-199a-5p agomir, or negative-control agomir for six weeks. Longitudinal inflammation, function, and ankle circumference ratio were assessed, followed by radiography, histology, OARSI scoring, ELISA, Western blotting, and RT-qPCR at week 8.ResultsThe fracture model caused persistent swelling and functional impairment, radiographic post-traumatic changes, cartilage surface disruption, proteoglycan depletion, increased IL-1β/TNF-α production, increased IHH/RUNX2/MMP-13 expression, and reduced SOX9/COL2A1 expression. miR-199a-5p agomir treatment partially improved function, reduced inflammatory scores and cytokine levels, lowered OARSI scores, and was associated with lower IHH expression and a less hypertrophic/catabolic marker profile. The negative-control agomir showed no comparable protective pattern.ConclusionsIntra-articular miR-199a-5p agomir attenuated experimental TAA-like cartilage degeneration. The protective phenotype was associated with reduced inflammation, lower IHH expression, attenuation of hypertrophic/catabolic marker expression, and partial restoration of cartilage matrix-related markers. Direct miR-199a-5p binding to IHH, downstream GLI activation, and local miRNA tissue accumulation were not tested and require further study. - Source: PubMed
Publication date: 2026/08/24
Fu ZhihongZhang YunhuiGuo HuiZhu RuizhengLi ZunwangLi DongxiaoMo XingjieChen ShaojiaBao ChangrenLu ZhongwenWei FangyuanChen Zhaojun - Does exposure to first-line chemotherapies affect the density and maturity status of testicular somatic cells from prepubertal to postpubertal males at the time of cryopreservation? - Source: PubMed
Publication date: 2026/08/23
Rousseau VRives NBasille-Dugay MNeusius CFraissinet FChemin EDufour MDupuis HRondanino CFeraille ADumont L - Primary liver cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), arise from the neoplastic transformation of hepatocytes and cholangiocytes, respectively. Loss or downregulation of PTEN, a tumor suppressor negatively regulating the PI3K/AKT pathway, is frequently observed in CCA and HCC. Notably, PTEN mutations are observed at nearly twice the frequency in combined CCA-HCC tumors than either HCC or CCA alone. Using lineage-specific liver-targeted PTEN-deficient mouse models, we demonstrate that PTEN loss drives cellular dedifferentiation and tumorigenesis, a process that is critically dependent on AKT2. Mechanistically, PTEN deficiency induces activation of NOTCH and upregulation of transcriptional factor SOX9, which plays a central role in tumor cell transformation. In parallel, PTEN loss increases SMAD4 expression and sensitizes the tumor cells to TGFβ signaling, with TGFβ treatment repressing SOX9 expression in tumor cells lacking PTEN. Together, our study defined a critical role for PTEN-AKT2 signaling in maintaining liver epithelial lineage fidelity and revealed how its disruption promotes the conversion of mature hepatocytes or cholangiocytes into liver cancer stem-like cells (LCSCs). Furthermore, we identify a PTEN-dependent crosstalk between NOTCH and TGFβ pathways that governs liver tumor development. Together, this work provides mechanistic insight into lineage plasticity in liver cancer with implications for pathway-directed therapy. - Source: PubMed
Publication date: 2026/08/20
Tang QiSlarve IelyzavetaChen JingyuZeng NiGu YiweiHe LinaHu ShunanAlhousari DialaXu ZifeiHua BrittneyZhang GuoNguyen PhillipAlba MarioBharadwaj AjayLee JihyeonKreimer SimionXu JianJi BaoanLu Shelly CVan Eyk JenniferChopra ShefaliKanel GaryYuan LiyunStiles Bangyan L - Prednisone is commonly used to control autoimmune and inflammatory diseases during pregnancy, but its potential effects on fetal skeletal development remain incompletely characterized. This study investigated the dose- and exposure-period-related effects of prenatal prednisone exposure (PPE) on fetal long-bone development in mice and explored the cellular mechanism involving chondrocyte-to-osteoblast transdifferentiation. Pregnant mice received prednisone at 0.25 or 1.0 mg/kg/day throughout gestation or 1.0 mg/kg/day during defined gestational periods. Fetal femurs were collected on gestational day 18 (GD18) for histomorphometric, histochemical, and immunofluorescence analyses. PPE shortened fetal femurs, reduced the primary ossification center (POC), narrowed the proliferative zone (PZ), and expanded the hypertrophic zone (HZ), with generally greater changes after higher-dose or longer-duration exposure. Quantitative cellular analysis demonstrated fewer proliferative chondrocytes, accumulation of hypertrophic chondrocytes, and reduced osteoblast numbers within the POC. Consistently, PPE decreased SRY-box transcription factor 9 (SOX9) and runt-related transcription factor 2 (RUNX2) protein expression while increasing type X collagen (COL10) expression. The accumulation of hypertrophic chondrocytes, together with insufficient osteoblast formation, indicates that PPE impairs the cellular transition from hypertrophic chondrocytes to osteoblasts. Collectively, impaired chondrocyte-to-osteoblast transdifferentiation represents a cellular mechanism contributing to PPE-induced fetal long-bone dysplasia. - Source: PubMed
Publication date: 2026/08/20
Zhu JiayongXiao HaoWang HuiChen Liaobin - The quality of cashmere fiber is fundamentally determined by the embryonic morphogenesis of hair follicles, a process highly dependent on the normal function of hair follicle stem cells (HFSCs). MicroRNAs (miRNAs) are key post-transcriptional regulators, but their specific roles in cashmere goat hair follicle development remain unclear. In this study, we identified the differentially expressed miRNA, miR-376c-3p, by analyzing transcriptomic data from embryonic skin (E65, E90, E120) of cashmere goats. Functional assays, including CCK8, crystal violet staining, clonogenic assay, and analysis of proliferation/apoptosis-related proteins (PCNA, CDK4, MKI67, BCL2, CAS3 and CAS9), demonstrated that miR-376c-3p significantly inhibited HFSCs proliferation, induced apoptosis, and blocked the differentiation process, as evidenced by the downregulation of differentiation-associated keratins (KRT4, KRT10, KRT14) and the upregulation of stemness maintenance factors (OCT4, NANOG, SOX9 and KRT15). Mechanistic investigations revealed that miR-376c-3p directly bound to the 3'UTR of STRBP mRNA and inhibited its expression, which was validated by a dual-luciferase reporter assay. Conversely, overexpression of STRBP promoted HFSCs proliferation and differentiation. Further analysis found that STRBP functioned by activating the Wnt/β-catenin and BMP signaling pathways, whereas miR-376c-3p inhibited these same pathways. In summary, this study elucidates a novel regulatory axis: miR-376c-3p influencing the Wnt/β-catenin and BMP signaling cascades in HFSCs by targeting STRBP mRNA, thereby regulating cell fate. This research provides important insights into the molecular mechanisms of miRNA-mediated hair follicle morphogenesis and stem cell biology in cashmere goats. - Source: PubMed
Guo YiWang NiuHou XiaojieSun LongkangHe HulinWang Xin