SOX9 pSer181
- Known as:
- SOX9 pSer181
- Catalog number:
- GTX23696
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9 pSer181
Related genes to: SOX9 pSer181
- 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 pSer181
Related articles to: SOX9 pSer181
- 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 - Despite notable advancements in autologous chondrocyte implantation (ACI) over the past three decades, persistent challenges including uneven cell distribution, low seeding density, and limited extracellular matrix formation continue to hinder outcomes. This study suggests a novel approach to matrix-assisted ACI (MACI) that integrates reactive jet impingement (ReJI) bioprinting with Chondro-Gide® (Ch-G) membranes to give an in theatre bioprinting approach with the potential to control cell distribution and density at the point of implantation. A collagen-alginate-fibrin (CAF) hydrogel was formulated as a bioink to maintain high cell viability and enable accurate deposition of chondrocytes at both low and high densities. Bone marrow-derived immortalised stem cells were differentiated into chondrocytes and bioprinted using the ReJI system onto Ch-G substrates. Constructs were evaluated over 14 days for cytotoxicity, morphology, gene expression, extracellular matrix (ECM) deposition, and mechanical properties. Live/dead assays confirmed high cell viability across all conditions. Immunofluorescence and scanning electron microscope (SEM) analyses showed enhanced cell alignment, surface migration, and ECM formation, particularly in high-density Chondro-Gide®/CAF samples (Ch-G/CAF). ACAN and SOX9 showed significant upregulation from day 1 to day 14 and immunohistochemical analysis confirmed robust deposition of collagen II and sulphated glycosaminoglycans (sGAGs). Mechanical testing demonstrated increased compressive modulus over time, with Ch-G/CAF constructs exhibiting superior stiffness and volumetric stability. These findings suggest that ReJI bioprinting of CAF hydrogels onto Chondro-Gide® membranes supports enhanced chondrogenic activity and matrix formation, offering a promising strategy for next-generation MACI. - Source: PubMed
Publication date: 2026/06/19
Ozdemir Steedman FatmaFerreira Ana MarinaMelo PriscilaDalgarno Kenneth - Chondrocyte proliferation, differentiation and hypertrophic mineralization are central events that guide subsequent vascular invasion and bone replacement processes. This process is controlled by a sophisticated molecular network including transcription factors such as SOX9 and Runx2, as well as key signaling pathways such as Bone Morphogenetic Protein (BMP), Indian Hedgehog (Ihh) and Fibroblast Growth Factor (FGF). Dysregulation of this network due to genetic mutations or metabolic deficiencies can disrupt mineralization, which underpins aberrant skeletal biomechanics properties. Therefore, understanding the physiological and pathological mechanisms governing chondrocyte proliferation, differentiation and mineralization holds significant potential for developing novel therapeutic strategies for disorders with compromised skeletal biomechanics. - Source: PubMed
Publication date: 2026/06/04
Liu YuhaoXu GuangyuShen YiFu ShaotianQin An - Turing patterns are a well-studied model of reaction-diffusion equations for developmental patterning. Their applicability has often been limited by the difficulty in identifying candidate molecules that satisfy the requisite criteria for patterning. Here, we build on recent work on geometric models to describe Turing patterning as a potential flow. We show how the universal dynamics of Turing patterning is described by a landscape, largely independent of the underlying reaction-diffusion equations. We apply our framework to three-component systems and demonstrate that we can accurately capture the dynamics of any given component. We extend our framework to larger networks and to models of Turing patterns coupled with external morphogens that provide positional information. We provide a quantitative description of the dynamics of chosen markers and apply it to the dynamics of SOX9 expression during digit patterning. - Source: PubMed
Shinde ShubhamRaju Archishman