Ask about this productRelated genes to: SOX9 antibody
- 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
Related articles to: SOX9 antibody
- KRAS is a common cancer-driving mutation that fuels the progression of several aggressive cancers, particularly pancreatic, colorectal, and lung cancers. Despite its well-established role in tumor development, effective therapeutic options that directly target KRAS remain limited. In this study, a structure-based virtual screening strategy was employed to identify potential KRAS inhibitors. Molecular docking was used to screen a library of traditional Chinese medicine (TCM) compounds, followed by ADMET (Absorption, Distribution, Metabolism, Excretion, and Toxicity) profiling. The top five drug-like candidates were subjected to 200 ns molecular dynamics simulations and MM-GBSA binding free-energy calculations. Three selected compounds were further evaluated in vitro, among which Rubimaillin showed notable anticancer activity with IC values of 1.10 ± 0.12 µM and 2.07 ± 0.02 µM against MIA PaCa-2 and PANC-1 cell lines, respectively, while displaying low toxicity toward non-tumorous HEK-293 cells (CC = 38.92 ± 8.49 µM). Rubimaillin also significantly inhibited cell migration and modulated key oncogenic biomarkers, including reduced KRAS protein levels, downregulation of BCL2, SOX9, and LC3 gene expression, and upregulation of p53 expression. Overall, these findings suggest that Rubimaillin may represent a suitable candidate for further investigation as a KRAS-targeted anticancer agent and demonstrate the value of integrating computational screening with natural product-based drug discovery approaches. - Source: PubMed
Publication date: 2026/04/26
Pandey DivyaDwivedi ShubhamRoy Kuldeep K - Epithelial plasticity allows committed cells to bypass rigid differentiation hierarchies, enabling efficient tissue repair through the reactivation of developmental-like programmes. In this review, we focus on the transcription factor SOX9 as a central regulator of epithelial cell fate rewiring. Essential during epithelial development and tissue morphogenesis, SOX9 is dynamically regulated across diverse epithelial tissues following injury, conferring SOX9-expressing cells with an increased 'stemness' and repair/regenerative capacity. Emerging evidence suggests that SOX9 may function as a molecular integrator of microenvironmental inputs during tissue perturbations. However, dysregulation or persistent activation of this programme carries inherent risks of fibrosis and malignancy. Future work aimed at understanding how SOX9 integrates biochemical and mechanical cues will be vital for developing strategies to harness the plastic potential of epithelial cells for regenerative medicine and prevent pathologies associated with this plasticity. - Source: PubMed
Publication date: 2026/04/24
Bejar Maria TAlcolea Maria P - - Source: PubMed
Publication date: 2026/04/24
Gould Poppy APetukhova Lynn - Autologous chondrocyte implantation (ACI) has long been regarded as the gold-standard chondrocyte-based therapy for articular cartilage repair. The main challenge in ACI is that chondrocytes lose their chondrogenic phenotype after monolayer expansion . The monolayer-expanded chondrocytes show dedifferentiation and senescence, hindering their ability to synthesize hyaline cartilage. Currently, there is no effective method to alleviate dedifferentiation and senescence in these monolayer-expanded chondrocytes. Adipose-derived stem cells (ADSCs) have been increasingly explored as a viable alternative cell source to chondrocytes for articular cartilage tissue engineering. Besides inducing chondrogenesis of ADSCs into chondrocyte, recent research emphasizes the positive impact of ADSC-secreted extracellular vesicles (ADSC-EVs). We demonstrate that ADSC-EVs alleviate dedifferentiation and senescence in monolayer-expanded chondrocytes, enhancing their capacity to produce hyaline cartilage. The ADSC-EVs treatment redifferentiated the monolayer-expanded chondrocytes by upregulating collagen type II (Col-II), sulfated glycosaminoglycan (sGAG), and SOX-9 expression and decreasing collagen type I (Col-I) levels. The redifferentiated chondrocytes also showed enhanced cell proliferation and reduced levels of P16 and senescence-associated β-galactosidase (SA-β-gal). Moreover, ADSC-EV treatment increased the ability of monolayer-expanded chondrocytes to synthesize hyaline cartilaginous matrices in 3D pellet culture. This effect is achieved through the suppression of interleukin-1β-induced mitogen-activated protein kinase (MAPK) signaling. Through next-generation sequencing and bioinformatic analyses, the miRNAs contained in ADSC-EVs were revealed as key candidates involved in mitigating dedifferentiation and senescence. Our findings propose a novel approach employing ADSC-EVs to restore the chondrogenic phenotype of monolayer-expanded chondrocytes, offering an alternative strategy for more effective ACI. - Source: PubMed
Publication date: 2026/04/25
Wu Shun-ChengChang Ling-HuaWu Che-WeiChen Chung-HwanChang Je-KenHo Mei-Ling - - Source: PubMed
Publication date: 2026/04/24
Choi Dong-JooMurali SanjanaKwon WookbongWoo JunsungSong Eun-Ah ChristineKo YeunjungSardar DebosmitaLozzi BrittneyCheng Yi-TingWilliamson Michael RHuang Teng-WeiSanchez KaitlynJankowsky JoannaDeneen Benjamin