SOX9 Mouse Monoclonal Antibody
- Known as:
- SOX9 Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006662-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SOX9 Mouse Monoclonal Antibody
Related genes to: SOX9 Mouse Monoclonal 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 Mouse Monoclonal Antibody
Related articles to: SOX9 Mouse Monoclonal Antibody
- Growth differentiation factor (GDF) 9 is a member of the transforming growth factor (TGF)-β superfamily, which plays an important role in mammalian ovarian follicular development and female fertility. However, its regulatory role in the male reproductive system remains largely unknown. - Source: PubMed
Jiang TiantuanGuo JinmingJiao YafeiXu MeinaHe JianLiu XiangyuQin GuangshengLiu XiaohongChen YaoshengCong PeiqingHe Zuyong - In addition to the purinergic receptor P2X7R's known activity as a sensor of damage-associated molecular patterns (DAMPs), evidences support its role in maintaining tissue homeostasis. Its presence in cellular compartments other than its usual transmembrane localization suggests its involvement in specific signaling pathways. This study aimed to analyze P2X7R in the nucleus of human chondrocytes and search for potential interacting partners. Through co-immunoprecipitation and proximity ligation assay we discovered that, independent of extracellular ATP levels, P2X7R is abundantly present in both the nuclear membrane and in the nucleoplasm, where it is found in close proximity to lamin A/C (a component of the nuclear lamina), emerin (a protein involved in the assembly and disassembly of the nuclear envelope), and SUN2 (an inner nuclear membrane protein that facilitates the transmission of mechanical forces). Furthermore, chromatin immunoprecipitation revealed the participation of P2X7R in molecular complexes located in the promoter of specific genes including Sox9, TRPS1, FOXO3a, integrin β2 and connective tissue growth factor. Overall, this evidence reveals for the first time novel partners of P2X7R that place it in an intricate network that influences nuclear structure, mechanosensitivity, chromatin organization, and gene expression. Specifically, on the one hand, a close association between P2X7R and nuclear proteins participating in the LINC (Linker of Nucleoskeleton and Cytoskeleton) complex (lamin A/C, emerin, and SUN2) places it among the factors involved in mechanosignaling and the maintenance of nuclear integrity; on the other, its recruitment to specific gene promoters suggests that it may act as a transcription regulator. - Source: PubMed
Publication date: 2026/06/17
Lambertini ElisabettaPenolazzi LetiziaChierici AnnaNadalini RiccardoSief ChiaraBegnozzi FrancescaBonora MassimoPinton PaoloBianchini Chiaradi Virgilio FrancescoPiva Roberta - Oncogenic condensates act as biophysical sanctuaries that stabilize malignant survival programs. However, a universal regulator capable of orchestrating the integrated biophysical axes governing cellular phase behavior has remained elusive. Here, we introduce a sovereign singularity framework, presenting a deductive biophysical model that positions the indoleamine melatonin as a master regulator of biological phase separation. A systematic synthesis and integrative bioinformatics analysis were performed to identify the intersection between melatonin-responsive genes and the phase-separation proteome. We identified a core 26-gene regulatory signature-including AR, BCL2, CGAS, CTNNB1, EP300, EZH2, EGFR, IKBKG (NEMO), KEAP1, KDM1A (LSD1), LEF1, MYC, NANOG, PRNP (PRP), SMAD3, SOX9, SQSTM1, TFEB, TFAM, TP53, TWIST1, USP10, WWTR1 (TAZ), VIM, YAP1, and YTHDF3-at the intersection of melatonin signaling and condensate architecture. We propose that melatonin utilizes a tri-lever framework of redox tuning (Lever I), multivalent plasticization (Lever II), and dielectric recalibration (Lever III) to render oncogenic programs biophysically untenable. This model provides a mechanical basis for high-resolution regulatory outcomes that modulate the organizational logic of nuclear decision-making (Axis I), state-transition (Axis II), and stress-adaptation (Axis III) condensates. Our results define a strategic platform for disrupting condensate-driven malignancy through the systemic modulation of the cellular biophysical landscape. - Source: PubMed
Loh DorisChuffa Luiz Gustavo de AlmeidaSeiva Fábio Rodrigues FerreiraReiter Russel J - SOX9 is a highly conserved transcription factor (TF) belonging to the SRY-related HMG-box (SOX) family and the high-mobility group (HMG) class of DNA-binding proteins. SOX9 integrates structural flexibility, DNA-dependent dimerization, and context-specific cofactor interactions to orchestrate organogenesis. In the pancreas, SOX9 acts as a dosage-sensitive gatekeeper: high expression in multipotent progenitors maintains proliferation and prevents premature endocrine differentiation, while its timely downregulation is a prerequisite for NEUROG3 (NGN3) induction and β-cell maturation. Genetic and clinical data from campomelic dysplasia and mouse models reveal that both haploinsufficiency and dominant-negative SOX9 variants disrupt pancreatic morphogenesis and endocrine formation, whereas inappropriate SOX9 reactivation in adult β-cells under metabolic or hypoxic stress drives dedifferentiation and diabetes-like phenotypes. Recent work further demonstrates that low-level SOX9 expression persists in mature β-cells, where it regulates alternative splicing and stress adaptation, underscoring its lifelong importance for β-cell function. Despite these insights, SOX9 has not emerged as a diabetes susceptibility gene in genome-wide association studies, suggesting that SOX9-related β-cell failure is primarily driven by rare, severe mutations and dysregulated expression rather than common variants. This review synthesizes current understanding of SOX9's multifaceted roles across pancreatic development and adult β-cell biology, highlighting conserved mechanisms established through mouse genetics, species-specific considerations for translating findings to humans, and emerging opportunities for therapeutic intervention targeting SOX9-dependent pathways to preserve β-cell function and identity in diabetes. - Source: PubMed
Publication date: 2026/06/17
Sharar NourEldaw MohamedIslam ZeyaulHabbab WesalAbdelalim Essam MKolatkar Prasanna R - Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine skin cancer with a poorly understood cell of origin and initiation process. Most MCC tumors feature monoclonal integration of Merkel cell polyomavirus (MCPyV) DNA, which expresses viral small T (sT-Ag) and large T antigens (LT-Ag), responsible for driving MCC tumors. The process by which MCPyV T antigens (T-Ags) transform cells to initiate MCC has been unclear, in part due to the lack of physiologically relevant in vivo models. Building upon our previous work, which demonstrated that SOX9-expressing (SOX9+) hair follicle Merkel cell progenitors are susceptible to T-Ag-mediated reprogramming, we establish a mouse model in which sT-Ag expression and Trp53 attenuation in SOX9 cells produce metastatic neuroendocrine tumors with histopathologic and immunophenotypic features of human MCC. Importantly, while sT-Ag alone induces partial MCC-associated gene expression, suppression of p53 is required for sT-Ag to induce neuroendocrine lineage transdifferentiation in the hair follicle. Cumulatively, these studies enhance our knowledge of MCC biology and establish a de novo MCC tumorigenesis model in a tractable immunocompetent system that will be invaluable for further advancements in the field. - Source: PubMed
Publication date: 2026/06/16
Weber MadisonAckermann AmandaLi Meng-YenMeehan Shane AEzhkova Elena