SOX9
- Known as:
- SOX9
- Catalog number:
- AP11363PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9
Related 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
- 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 - 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