SOX9
- Known as:
- SOX9
- Catalog number:
- ARP37986_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9
Ask about this productRelated 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
- - Source: PubMed
Publication date: 2026/04/20
Yang Han-Mo - Intervertebral disc degeneration (IVDD) is a major contributor to low back pain and is characterized by mitochondrial dysfunction, inflammation, and regulated cell death in nucleus pulposus (NP) cells. NLRP3 inflammasome-mediated pyroptosis plays a pivotal role in disc degeneration, whereas mitophagy limits mitochondrial damage and inflammasome activation. Emerging evidence indicates that pterostilbene (PTE) exhibits diverse pharmacological activities; however, its role in attenuating IVDD remains insufficiently understood. - Source: PubMed
Publication date: 2026/06/17
Zhang YangLiu ShuanggongDong ShuhangSong GuangxuWang KewenZhou ZhiYang GuoweiYang XuPeng ShuaiZhang YingzeWu Dongjin - DAX-1 (NR0B1) is a pivotal regulator of mammalian reproductive and endocrine development. Discovered as a gene whose dosage imbalance can reverse sex in XY individuals, DAX-1 is now recognized as a key component of the network controlling gonadal formation and function. Despite decades of research, the molecular mechanisms of its function in gonad development and function remain only partially understood. We combine genetic, developmental, molecular and biochemical perspectives to present how DAX-1 regulates gene expression from early sex determination and gonadal differentiation to the maintenance of steroidogenic homeostasis in adrenal and gonadal tissues. Recent advances have reshaped our view of DAX-1 beyond its classical role as a transcriptional repressor. Evidence shows that it functions within dynamic transcriptional networks, interacting with regulators such as SF-1 (NR5A1), SOX9 and other nuclear receptors to fine-tune gene expression in a context-dependent manner. Genomic, structural, and proteomic studies reveal that DAX-1 participates in complexes integrating developmental and hormonal cues, coordinating differentiation and steroidogenesis. Moreover, its emerging roles in RNA-associated gene regulation broaden its functions beyond canonical nuclear receptor signaling. We revisit DAX-1 contribution to sex determination and differentiation from an evolutionary and mechanistic viewpoint, emphasizing its interactions with the SRY-SOX9 axis and its dosage-sensitive influence on gonadal fate. The developmental and clinical consequences of DAX-1 mutations and copy number variations manifest as a spectrum of human phenotypes, from adrenal hypoplasia congenita to differences/disorders of sex development (DSD), highlighting its essential role in maintaining endocrine balance. - Source: PubMed
Publication date: 2026/06/20
Bardoni BarbaraLalli Enzo - Understanding sex determination mechanism is crucial for elucidating sexual evolution and sex control in animal husbandry. In this study, data showed that doublesex and mab-3 related transcription factor 2 (DMRT2) expression in gonads was developmentally regulated in a sex- and lateralization-specific manner. The nuclear localization signal of DMRT2 was identified, showing high expression in the female gonadal cortex. Transcriptome and chromatin immunoprecipitation followed by sequencing (ChIP-seq) analyses screened and validated target genes (component of inhibitor of nuclear factor kappa B kinase complex (CHUK) and SRY-box transcription factor 9 (SOX9)) and downstream signaling pathways (e.g., sex determination, cell apoptosis, and inflammation related). It was also validated that DMRT2 could promote cell proliferation and inhibit apoptosis. The effect of DMRT2 on apoptosis and inflammation was mediated by CHUK. These factors may potentially regulate apoptosis pathway and Wnt signaling pathway. In conclusion, DMRT2 participates in sex differentiation and development of chicken gonads by regulating proliferation, apoptosis, and inflammatory pathways through target genes such as CHUK and SOX9. The novel mechanism of DMRT2 regulating avian gonadal differentiation and development may deepen understanding of vertebrate sexual evolution and facilitate sex control in poultry. - Source: PubMed
Publication date: 2026/05/25
Lin XiaoJin ZidiImtiaz AneeqaGe JingGong HaizhouZhang YihuiZheng YunZhao MinmengGong DaoqingLiu LongGeng Tuoyu - Bisphenol S (BPS) has emerged as a common substitute for bisphenol A in various consumer products. However, growing evidence suggests that BPS is an endocrine disruptor with potential impacts on thyroid hormone (TH) regulation and testicular function. This study aims to assess the impact of thyroid disruption on testicular development following maternal exposure to BPS. Pregnant and lactating female Wistar rats were treated with either BPS or AT 1-850 (a thyroid hormone receptor antagonist). Testicular development was evaluated at gestational day 20 (GD20), postnatal day 21 (PND21), and postnatal day 35 (PND35) through histology, testosterone quantification, and assessments of SOX9 and CYP17A1 expression in Leydig and Sertoli cells at both protein and gene levels. BPS exposure significantly reduced body weight and relative testes weight in male offspring (PND21 and PND35), accompanied by a decrease in anogenital distance, serum testosterone levels and seminiferous tubule diameter, along with histopathological alterations of the tubules. Additionally, the development of the offspring's testes appears to be impaired following BPS exposure, as evidenced by the lower expression of two key factors, namely SOX9 and CYP17A1, at both protein and molecular levels. It is also important to note that the majority of the deleterious effects of BSP are also similarly observed following treatment with AT 1-850. Based on the consistent results between the BPS and AT 1-850-treated groups, we conclude that BPS disrupts testicular development in male offspring by blocking nuclear THRs following maternal exposure during both fetal and postnatal stages. - Source: PubMed
Publication date: 2026/06/19
Rhouma Mariem BenChouchene LinaVenditti MassimoBoughammoura SanaKessabi KaoutharMessaoudi Imed