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
- Intestinal aging is characterized by impaired intestinal stem cell (ISC) function, reduced mucosal regenerative capacity, and progressive epithelial barrier deterioration. However, the upstream metabolic and epigenetic mechanisms that regulate ISC homeostasis during aging remain poorly understood. This study aimed to determine how SIRT6 regulates ISC homeostasis during intestinal aging and to investigate whether Atractylenolide II (AT-II) can alleviate age-related ISC dysfunction. Jejunal tissues from young and aged mice, intestinal epithelial-specific Sirt6-deficient mice, and 3D intestinal organoids were used to evaluate crypt-villus morphology, ISC activity, and lineage differentiation. Mechanistic analyses included western blotting, immunofluorescence, and retinoic acid (RA) quantification, complemented by pharmacological and rescue experiments targeting RXRα activity and RA metabolic balance. The results showed that SIRT6 protein expression was markedly reduced in the aged jejunum, correlating with a decreased villus-to-crypt (V/C) ratio, impaired ISC proliferation, and altered epithelial differentiation. Intestinal epithelial deletion of Sirt6 recapitulated aging-related intestinal defects, including crypt atrophy and ISC-associated dysfunction. Consistently, aged organoids displayed reduced SIRT6 protein expression, while Sirt6 organoids showed decreased SOX9 and Lgr5 expression. Mechanistically, SIRT6 physically associated with RXRα, and SIRT6 loss or inhibition was associated with increased RXRα acetylation, elevated RXRα abundance, and RA metabolic remodeling. These changes were accompanied by disrupted RA balance and aging-like ISC dysfunction. AT-II partially restored SIRT6/RXRα/RA-related molecular alterations and alleviated ISC-associated dysfunction. This study suggests that the SIRT6/RXRα/RA axis contributes to ISC homeostasis during intestinal aging and may be modulated by AT-II, offering a potential strategy for age-related intestinal barrier damage. - Source: PubMed
Publication date: 2026/08/27
Cao YaqianSong ChunhuiSun XiaoqingNiu ZhenyuZhang XueniQi KerongCai JiazhongGuo WenfengChen GangLi NingLi Yanwu - Intervertebral disc (IVD) degeneration, a leading cause of chronic lower back pain, is associated with loss of vacuolated notochordal cells (NCs) and fibrotic remodeling of the nucleus pulposus. Emerging therapies increasingly focus on NCs, which are rare but therapeutically relevant cells for regenerating degenerated IVDs. In this study, we used CRISPR-based transactivation (CRISPRa) to direct the differentiation of human induced pluripotent stem cells (iPSCs) into the NC lineage. We tested CRISPRa-mediated activation of NOTO, TBXT, FOXA2, SOX5, SOX6, and SOX9, coupled with single-cell sequencing of Aggrecan-2A-mScarlet reporter iPSCs. This approach identified the SOX5/6/9 combination (SOX-trio) as critical for promoting NC lineage commitment. The SOX-trio yielded the largest cell population expressing a range of genes previously associated with NC identity, including SHH, FOXA1, FOXA2, FOXJ1, FN1, ALCAM, KRT8, and KRT18. Our study demonstrates the integration of CRISPRa with single-cell technologies as a powerful platform for investigating and enriching iPSC-derived NCs, supporting future regenerative strategies across various fields. - Source: PubMed
Publication date: 2026/08/27
Tong XiaoleVisscher MariekeRiemers Frank MVersluis DanielleGeijsen NielsShang PengTryfonidou Marianna APoramba-Liyanage Deepani W - Tumour-associated macrophages (TAMs) are known to promote tumour progression in many kinds of malignant tumour, including hepatoblastoma (HB). Based on previous studies, we suggested that TAM-mediated sex-determining region Y-box 9 (SOX9) signal might enhance HB progression. The present study investigated the significance of the SOX9 signal in HB and examined the mechanisms underlying cell-cell interactions between tumour cells and TAMs. Co-culture with human monocyte-derived macrophages increased SOX9 expression in HB cell lines. Immunohistochemical analysis of HB samples revealed a positive correlation between SOX9 expression and TAM infiltration, and SOX9 expression was predominantly observed in the embryonal subtype. Increased SOX9 expression was associated with shorter 5-year recurrence-free and overall survival. Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signalling was found to be involved in macrophage-induced SOX9 upregulation. The Wnt/β-catenin pathway was also activated by co-culture with macrophages and appeared to be upregulated by SOX9 expression. In summary, SOX9 was identified as a poor prognostic factor in HB, with expression enhanced by macrophage-derived factors. The YAP/TAZ and Wnt/β-catenin pathways are critical for cell-cell communication and are linked to SOX9 overexpression. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/08/27
Hirao HirokiAdawy AhmadFujiwara YukioYoshii DaikiPan ChengLi LianboYano HiromuKondo YoshihikoHonda MasakiHan JiaLiu YaoYamada SohsukeHiyama EisoChunthaboon PaweenaponSakamoto YasuhisaMoroishi ToshiroYamamoto MasahiroHibi TaizoKomohara Yoshihiro - Hidradenitis suppurativa (HS) is increasingly recognized as a disorder of intrinsic dysregulation at the intersection of genetic susceptibility, host-microbial interactions, and hormonal signaling, with select environmental exposures acting as important secondary modifiers. This narrative review synthesizes mechanistic, clinical, and epidemiologic evidence on intrinsic and extrinsic contributors to HS pathogenesis. Genetic susceptibility for HS involves pathways regulating keratinocyte differentiation, epidermal stem cell function, and follicular architecture, including Notch signaling and transcriptional regulators such as SOX9 and KLF5. Microbiome alterations in both lesional and non-lesional skin suggest that early dysbiosis may contribute to follicular occlusion, epithelial disruption, and immune activation. Hormonal signaling, particularly androgen signaling, promotes follicular dysfunction and inflammation during periods of hormonal fluctuation, frequently aligning with the time of disease onset and flares. Environmental exposures vary considerably in the strength of supporting evidence: tobacco use and elevated body mass index have the most robust epidemiologic and mechanistic data, heat and humidity are increasingly recognized as disease activity modifiers, and evidence for air pollution and microplastics is growing. Collectively, these findings support a model in which HS arises from intrinsic follicular dysregulation shaped by genetic, microbial, and hormonal factors, with environmental exposures influencing but unlikely to independently initiate disease. - Source: PubMed
Publication date: 2026/08/13
Moslehi DorsaJohnson LannikaCharrow Alexandra PPastar Irena - Neuropathic pain (NP) is a debilitating chronic condition whose molecular mechanisms remain incompletely understood, limiting the development of effective disease-modifying therapies. Lactylation, a lactate-derived post-translational modification of histone and non-histone lysine residues, has recently emerged as a critical epigenetic mechanism that directly couples glycolytic activity to transcriptional reprogramming. Following peripheral nerve injury, four pain-relevant cell populations undergo cell-type-specific glycolytic reprogramming through distinct upstream cascades: the AREG-EGFR-PKM2 axis in dorsal root ganglion sensory neurons, RUNX1-CMPK2 in spinal microglia, Sox9-HK1 in spinal astrocytes, and LDHA in peripheral Th17 cells. The resulting intracellular lactate accumulation drives lactylation through three mechanistic modes: transcriptional activation of pro-nociceptive genes, silencing of analgesic mediators, and direct inactivation of pain-suppressive signaling proteins. A self-reinforcing feedback loop between glycolysis and lactylation further perpetuates the chronic pain state. This review synthesizes current mechanistic evidence, evaluates emerging pharmacological strategies targeting this metabolic epigenetic axis, and discusses outstanding translational challenges including reader protein identification, sex-based variability, and human tissue validation. - Source: PubMed
Publication date: 2026/08/26
Qin ZhengshanZeng YuanOu Cehua