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
- DNA mismatch repair (MMR) maintains genomic stability, and defects in MMR genes such as MLH1 and MSH2 predispose to cancer. Unlike other MMR components, MLH1 has unexplained roles in development, as Mlh1-deficient male mice exhibit severe testicular hypoplasia and sterility. Here, we uncover that MLH1 regulates testis development through the Hippo-Yes-associated protein (YAP) pathway. MLH1 directly binds YAP via its C-terminal domain and the WW domains of YAP, competitively inhibiting LATS1-mediated YAP phosphorylation. This interaction stabilizes YAP by suppressing ubiquitination and promotes its nuclear translocation dependent on MLH1's nuclear localization signal. Additionally, MLH1 facilitates YAP-TEAD complex formation, enabling expression of testicular development genes, including Wt1, Sox9, and Ctgf. These functions are independent of the MMR activity of MLH1. Mlh1-deficient mice show elevated YAP phosphorylation, reduced target gene expression, and impaired proliferation in developing testes. Pharmacological inhibition of the Hippo pathway kinases MST1/2 partially rescues testis hypoplasia in Mlh1-/- mice. These findings establish MLH1 as a Hippo pathway regulator and resolve its long-standing role in male gonad development. - Source: PubMed
Li XueyingYang JiajunLi Guo-Min - Engineering hydrogels that simultaneously provide interconnected porosity for cell infiltration while delivering appropriate mechanical cues to direct stem cell fate remains a critical challenge in cartilage tissue engineering. Herein, we report a biomimetic COL-HA-PVA hydrogel scaffold with systematically tunable pore sizes (1.2, 1.4, and 1.6 mm) and concomitant mechanical properties, enabling the co-regulation of the structural and biomechanical microenvironment. The 1.2 mm scaffold exhibited the lowest and most stable compressive modulus across the physiologically relevant strain range, providing a compliant mechanical microenvironment that promoted BMSC chondrogenesis, coupled with enhanced surface hydrophilicity due to collagen functionalization. In vitro, this optimized pore architecture significantly promoted goat bone marrow mesenchymal stem cell (gBMSC) adhesion, spreading, and sustained proliferation over 14 days. More importantly, the 1.2 mm scaffold directed robust chondrogenic differentiation, as evidenced by markedly increased expression of the genes and proteins SOX9, COL-II, and aggrecan relative to larger-pore counterparts. Mechanistically, the scaffold activated the integrin β1-FAK-RhoA/ROCK mechanotransduction axis to enhance SOX9-mediated transcription while suppressing osteogenic markers RUNX2 and COL-I. In a caprine model of full-thickness osteochondral defects, the BMSC-laden 1.2 mm scaffold achieved seamless integration with host tissue, progressive subchondral bone regeneration, and formation of proteoglycan-rich hyaline-like cartilage, as confirmed by micro-CT, histological staining, and GAG quantification. This work demonstrates that synergistic tuning of pore architecture and mechanical properties represents a powerful design strategy for directing stem cell-based cartilage regeneration, offering mechanistic insights into scaffold-guided cell fate determination. - Source: PubMed
Publication date: 2026/09/08
Chen PengLu WeiWang HaoyiLiu TianhuaJiang QihongYang LingchenHu Yihe - The repair of osteochondral defects is challenging due to differing regenerative capacities of bone and cartilage, a challenge that is often exacerbated by chronic inflammation. This study evaluated the immunomodulatory and regenerative potential of hydroxyapatite (HAp), β-tricalcium phosphate (β-TCP), graphene oxide (GO), and zinc oxide (ZnO) on osteoblast-like cells (Saos-2) and chondrocyte-like cells (SW1353) under IL-1β-induced inflammatory conditions. An MTT assay was used to measure cell viability at different concentrations of substances. To investigate the ability of Saos-2 cells to synthesize an inorganic extracellular matrix (ECM), mineralisation was observed via Alizarin Red staining and alkaline phosphatase (ALP) activity. The protein production of pro-COL1, pro-COL2, ACAN, MMP-9, IL-6, IL-8, BMP-2/4, RUNX2, and SOX9 was assessed using ELISA and Western blotting. The gene expression of RUNX2, SOX9, MMP-3, ADAMTS-5, COL10A1, ACAN, BGLAP, and FGF-2 was evaluated using RT-qPCR. Under inflammatory conditions, all the evaluated substances maintained basal matrix synthesis while suppressing the expression of ECM-degrading enzymes. Notably, GO exhibited a strong chondroprotective effect in SW1353 cells by significantly downregulating the expression of RUNX2 and FGF-2. Conversely, ZnO was found to impair mineralisation via the cytoplasmic trapping of RUNX2. Furthermore, their distinct impact on cellular phenotypes, ranging from GO-mediated chondroprotection to the inhibition of mineralisation by ZnO, highlights that the strategic, layer-specific integration of these substances is essential for actively guiding and sustaining the complex process of osteochondral healing. Consequently, our findings demonstrate a dual therapeutic benefit, in which the evaluated substances simultaneously suppress ECM degradation and support fundamental matrix synthesis under inflammatory stress. - Source: PubMed
Publication date: 2026/09/08
Novotný RomanRajzer IzabellaFranková Jana - Periodontal diseases and temporomandibular disorders are characterized by chronic inflammation and progressive destruction of supporting tissues, leading to functional and aesthetic impairments. In this context, regenerative dentistry has increasingly focused on minimally invasive strategies capable of restoring tissue structure and function. Mesenchymal stem cells (MSCs) have emerged as central elements of regenerative approaches due to their multilineage differentiation potential, immunomodulatory properties, and paracrine activity. Concurrently, low-level laser therapy (LLLT), also known as photobiomodulation (PBM), has gained relevance as a non-invasive modality capable of modulating cellular behavior, inflammation, and tissue repair. This scoping review synthesizes current evidence on the combined application of MSCs and light-based therapies, emphasizing how laser-mediated metabolic modulation influences MSC fate and regenerative outcomes. Overall, the findings demonstrate that PBM enhances MSC proliferation, viability, migration, and lineage-specific differentiation, osteogenic, chondrogenic, angiogenic, and adipogenic, in a wavelength-, energy-, and dose-dependent manner. Emerging evidence indicates that the mitochondrial function represents a critical mechanistic link between laser irradiation and MSC responses. Photobiomodulation modulates mitochondrial bioenergetics primarily through activation of cytochrome c oxidase, resulting in increased ATP production, controlled reactive oxygen species signaling, and regulation of key transcription factors such as RUNX2, Sox9, and PPARγ. These mitochondrial-mediated effects act as metabolic checkpoints that integrate microenvironmental cues with lineage commitment and tissue-specific regeneration. Collectively, the data support the concept that precise modulation of mitochondrial activity by PBM optimizes the regenerative potential of MSCs. A deeper understanding of the interplay between laser strategies and parameters, mitochondrial metabolism, MSC source, and the cellular microenvironment is essential for the development of safe, effective, and reproducible regenerative protocols in dentistry and regenerative medicine. - Source: PubMed
Publication date: 2026/09/08
de Mattos Ygor Gonçalves Felixde Melo Otávio Augusto Alfonso MoraisFerreira José Ricardo MunizShibli Jamil AwadBezinelli Letícia MelloEduardo Fernanda de PaulaFaria Alessandra V SBueno Daniela Franco - Spermatogenesis is a tightly regulated process that involves an orchestrated transcriptional and translational event across the seminiferous epithelium. While individual regulators of this process have been studied, the network-level dynamics underlying the transition from spermatogonial stem cells (SSCs) to round spermatids (RSs) remain poorly understood. The dynamic molecular transitions between SSCs and RSs have not been fully characterised, particularly at the network level. Therefore, this study aimed to characterise the molecular and network-level dynamics underlying the transition from SSCs to RSs by integrating transcriptomic profiling, protein-protein interaction network analysis, functional enrichment, and immunohistochemical validation. - Source: PubMed
Publication date: 2026/08/08
Qorbanee AliAzizi HosseinFadhil Alsaffar MarwaSkutella Thomas