SOX9
- Known as:
- SOX9
- Catalog number:
- AP15791PU-N
- Product Quantity:
- 1.0 ml
- 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
- Lung adenocarcinoma (LUAD) shows extensive lineage plasticity and early metastatic dissemination, but the oncogenic events that actively drive these processes remain poorly defined. Here, we identify coordinated PRKCI and ECT2 copy number gain, present in approximately 30% of human LUADs, as a driver of developmental reprogramming and metastasis. Using a genetically engineered mouse model that recapitulates PRKCI-ECT2 gain in Kras/Trp53-driven LUAD, we show that elevated PKCι-ECT2 signaling rewires tumor trajectory in a cell-of-origin-dependent manner. Alveolar type II cell-derived tumors dedifferentiate into a distal SOX9 progenitor-like state associated with aggressive growth and liver metastasis, whereas club cell-derived tumors transition into a foregut SOX2 progenitor-like state that supports lineage infidelity and histological transformation. Human LUAD analyses support these progenitor programs as clinically relevant features of PRKCI-ECT2 gain. - Source: PubMed
Publication date: 2026/07/18
Nguyen Duy TMeneses Kayleah MZhang ChengPrieto Luis IWeems CapellaJamieson LeeLi HuBaker Darren JKhoor AndrasMurray Nicole RJustilien VerlineFields Alan P - Acetyl-CoA is a central metabolite that links energy status to transcriptional regulation through protein acetylation, yet its functions in skeletal biology depend strongly on subcellular compartmentalization. Because acetyl-CoA does not freely traverse biological membranes, its mitochondrial, cytosolic, and nuclear pools are maintained through compartment-specific synthesis and exchange routes, including the citrate-SLC25A1-ACLY axis, acetylcarnitine/carnitine cycling, acetate-dependent ACSS2 activity, and local nuclear enzyme activity. This review synthesizes current evidence that three conserved modules, including glycolytic/PDC-driven mitochondrial production, CIC/ACLY-mediated citrate export, and HAT-dependent acetylation, connect carbon flux with skeletal cell fate. However, lineage-specific outcomes are shaped by local acetyl-CoA availability, acetyltransferase context, and the transcription-factor landscape, including RUNX2 (osteogenesis), SOX9 (chondrogenesis) and NFATc1 (osteoclastogenesis). Critically, compartmentalized acetyl-CoA dysregulation can contribute to different pathological states: excessacetyl-CoA supply is linked to ACLY/FAO-driven cartilage catabolism and osteoclast resorption, whereas insufficient nucleocytosolic supply is associated with impaired regenerative programs in aged or inflamed bone. This duality argues for context-specific therapeutic strategies that either restrain excess acetyl-CoA flux or restore deficient pools. We propose that the translational bottleneck is not target identification but delivery precision, advocating for localized metabolite supplementation, cell-selective ACLY/FAO inhibitors, and spatial acetylome mapping to deconvolute cell-type-specific fluxes. Moving beyond broad HDAC/HAT modulation toward compartment-resolved strategies will be essential for translating acetyl-CoA biology into effective skeletal therapies. - Source: PubMed
Publication date: 2026/07/17
Yang QianyuShi RunlinZhang ChenyangSun WeiChen Guangjin - Osteoarthritis (OA) is a chronic, debilitating degenerative joint disease whose prevalence is rising markedly with the rapid aging of the global population. In this study, we investigated the chondroprotective efficacy of NP-2007, an enzymatically hydrolyzed low-molecular-weight collagen from , using IL-1β-stimulated SW1353 human chondrocyte cells and a medial meniscal transection (MMT)-induced OA rat model. In SW1353 cells, NP-2007 considerably suppressed the expression of inflammatory mediators (iNOS, COX-2) and cytokines (TNF-α, IL-6) without cytotoxicity. Crucially, it restored matrix homeostasis by downregulating catabolic enzymes (MMP-3, MMP-13, and ADAMTS-5) and upregulating anabolic markers (COL2A1, aggrecan), a process associated with the modulation of the Wnt/β-catenin and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathways and the recovery of the master chondrogenic factor SOX9. These in vitro findings were consistent with the in vivo results from the MMT model, where oral administration of NP-2007 (50 and 200 mg/kg) for 8 weeks effectively preserved articular cartilage structure and proteoglycan content while markedly reducing serum levels of catabolic biomarkers, including MMP-13 and COMP. Collectively, our findings demonstrate that NP-2007 exerts potent chondroprotective effects by modulating the balance between cartilage degradation and synthesis, suggesting its potential as a therapeutic candidate for the management of OA. - Source: PubMed
Publication date: 2026/06/26
Kim Min JuLim Hyeon-JiPark In-SunChoi BongsukKim TaeheeCho HyoungKwonKim Seon-YoungJung Chan-Hun - Endometrial organoids, with their three-dimensional structure and robust hormonal responsiveness, have emerged as valuable models for investigating uterine physiology and embryo implantation. However, conventional derivation from endometrial biopsies is invasive, carries surgical risks, and limits repeated sampling. This study introduces uterine lavage fluid as a non-invasive source for generating endometrial organoids. - Source: PubMed
Publication date: 2026/07/14
Qiu HuiyuFan ZhiwenLiu DiDeng LiWang XiaoxiaYang YuanyuanYang TianliTian FenHao JieZhang QiongXu BinFu JingNi HuilingLi YinshuangSu HankunXiao FenSun YuanyuanChen JingjingDuan ZhiyingZhao JingLi HuiLi Yanping - Gastric cancer develops through a sequential carcinogenic process beginning with pyloric metaplasia, a key feature of which is the transdifferentiation of gastric chief cells into spasmolytic polypeptide-expressing metaplastic (SPEM) cells. We found that SOX9, a transcription factor, is highly expressed in SPEM cells in both human and murine metaplasia. We therefore investigated the impact of SOX9-mediated SPEM cell plasticity and function on metaplasia development and progression during gastric carcinogenesis. - Source: PubMed
Publication date: 2026/07/14
Guenther Alexis ARuelas AmandaCaldwell BriannaCho YoungwonZhang ChangqingJang BogunDuncan Benjamin CRomero-Gallo JudithBusada Jonathan TPeek RichardChoi Eunyoung