SOX9 Control Peptide
- Known as:
- SOX9 Control Peptide
- Catalog number:
- AP11362CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9 Control Peptide
Related genes to: SOX9 Control Peptide
- 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 Control Peptide
Related articles to: SOX9 Control Peptide
- Fasting enhances small intestinal regeneration after radiation, but the contribution of the gut microbiome to this process remains uncharacterized. We identify () as a key mediator of this response. was enriched in fasted mice and its antibiotic depletion abrogated radioprotection, whereas reintroduction restored both organismal survival and intestinal integrity. Fasting elevated propionic acid, consistent with 's metabolic output. -conditioned medium and propionate induced histone H3 acetylation in intestinal stem cell cultures while in vivo fasting induced -dependent H3K27ac and H3K9ac, remodeling promoter-enhancer landscapes in crypt epithelial cells. Epigenetic profiling revealed a rewired core regulatory program enriched for pioneer transcription factors (Foxa, Gata, Klf), architectural organizers (Ctcf, Boris), and lineage-defining and metabolic regulators (Cdx2, Hnf4). This program supports expansion of a population of primed persister cells characterized by open chromatin accessibility at key stem and regenerative-associated loci including , , These findings define a fasting-induced microbiome-metabolite-chromatin axis that epigenetically primes highly plastic persister cells for rapid regeneration of the intestinal epithelium following radiation-induced injury. - Source: PubMed
Publication date: 2026/06/23
Barrodia PraveenSaw Ajay KumarJeter-Jones Sabrina LChang Chia-ChiShao JiansuArslan EmreSingh Anand KSatpati SureshJenq Robert RRai KunalPiwnica-Worms Helen - The interaction between injured proximal tubular epithelial cells (PTECs) and the microenvironment has been widely associated with post-AKI fibrosis; however, the underlying mechanisms remain largely unclear. In this study, we identified three distinct injury patterns of the tubular basement membrane (TBM) in kidney tissues from patients with acute kidney injury. Phosphorylated H3 and transforming growth factor-β1 (TGFB1) were co-localized in PTECs exhibiting TBM injury. To mimic this condition, we employed a low-attachment culture system (LACS). LACS induced in PTECs a morphology resembling that of maladaptive repaired PTECs, accompanied by G2/M cell-cycle arrest, as well as upregulation and secretion of TGFB1. The expression of TGFB1 was markedly suppressed when PTECs were re-attached to normal culture dishes or to medium supplemented with Matrigel. Furthermore, TGFB1 expression was not directly linked to G2/M arrest in PTECs. Mechanistically, knockdown of TGFB1 or SMAD3 attenuated the LACS-induced upregulation of SOX9, whereas SOX9 knockdown did not downregulate TGFB1 expression. We further demonstrated that TBM injury-induced upregulation of TGFB1 is mediated by ETV5. Collectively, these findings indicate that TBM damage triggered by AKI promotes renal fibrosis via activation of the ETV5/TGFB1/SMAD3/SOX9 pathway in proximal tubular epithelial cells following AKI. - Source: PubMed
Publication date: 2026/06/22
Dier AMina KaZhou WeiranSong NanaJin ShiShen ZiyanTan XiaoZhang LiwenCai JieruLi FangLi YangLi JieLu YufeiZhang WeidongChen YafeiDing XiaoqiangZhao Shuan - Intervertebral disc degeneration (IDD) is frequently associated with chronic low back pain (LBP), which contributes significantly to disability, psychological distress, and reduced work capacity. Mesenchymal stromal cell (MSC)-based treatments may offer a promising, less invasive alternative to conventional treatments for IDD. The MSC secretome has shown regenerative potential through paracrine and anti-inflammatory mechanisms. In this study, we investigated the effects of the secretome isolated from interleukin-1β (IL-1β)-preconditioned bone marrow-derived MSCs (BM-MSCs) on human nucleus pulposus cells (hNPCs) adopting a 3D in vitro culture model. - Source: PubMed
Publication date: 2026/06/20
Tilotta VeronicaVadalà GianlucaAmbrosio LucaDi Giacomo GiuseppinaCicione ClaudiaRusso FabrizioPapalia RoccoDenaro Vincenzo - The expression and secretion of sulfated colonic-type mucins is a feature of high-risk metaplasias of the gastrointestinal foregut (Barrett's esophagus, type III intestinal metaplasia of the stomach, and pancreatic intraepithelial neoplasia). Galectin-3 is a lectin that preferentially associates with galactose modified by a 3'-O-sulfate relative to its unmodified counterparts and is upregulated as the tissue transitions to high-risk metaplasia, dysplasia, and cancer. Since both galectin-3 and sulfated glycotopes are aberrantly and concurrently overexpressed in high-risk premalignant and malignant tissue transformations, we sought to investigate the role of galectin-3 in the metaplastic reaction. We found that injury induces the expression of at the RNA and protein levels. Unlike cancer cell lines, we show that galectin-3 colocalized with sulfomucins in zymogenic granules of the gastric chief cell. Utilizing a synchronous, chemically-induced murine model that produces spasmolytic polypeptide expressing metaplasia, we found that galectin-3 facilitates cathartocytosis of the vesicles it resides in, but not organelles lacking LGALS3. Inhibition of cellular downscaling resulted in delayed expression of the metaplastic transcription factor Sox9 as well as proliferation. Here, we present a new role for galectin-3 in promoting the transition from normal, homeostatic tissue to metaplasia and our data suggest that cathartocytosis represents an unconventional secretory pathway for galectin-3, which has been a matter of controversy as galectins are not secreted via canonical pathways. - Source: PubMed
Publication date: 2026/06/11
Lin XiaoboLiu XuemeiNicolazzi GabrielPan AnnieHua MargaretBrown Jeffrey W - Osteoarthritis (OA) is a joint disease characterized by age-related cartilage degradation, synovial inflammation, and imbalanced macrophage polarization. Pro-inflammatory cytokines, such as IL-1β and TNF-α, play critical roles in the progression of OA. Current treatments provide symptomatic relief but fail to address the underlying pathophysiological mechanisms, necessitating innovative therapeutic strategies. In this study, engineered macrophage membrane-incorporated hyaluronic acid methacrylate hydrogel microspheres (EMM@HMs) were used to neutralize pro-inflammatory cytokines and promote cartilage repair in osteoarthritic joints. The EMM@HMs were prepared using microfluidic techniques and characterized using scanning electron microscopy (SEM), zeta potential analysis, and particle size analysis. Cartilage organoids were prepared as a three-dimensional model to simulate native cartilage. The anti-inflammatory and cartilage-protective effects of the EMM@HMs were evaluated in vitro and in rats with OA. Results demonstrated that EMM@HMs neutralized IL-1β and TNF-α, promoted M2 macrophage polarization, and reduced cartilage degradation in cartilage organoids and OA rats. The EMM@HMs upregulated extracellular matrix (ECM)-related genes (COL2A1 and SOX9) and suppressed catabolic markers (MMP13 and COL10A1), highlighting their role in regulating ECM remodeling and chondrocyte differentiation. These findings demonstrated the potential of EMM@HMs to target inflammatory and degenerative pathways, offering a promising strategy for OA treatment. - Source: PubMed
Publication date: 2026/06/11
Ma ChenggongXiao ZhishengMa YetianJiang WenweiQian YufanDeng ZichengGuo Jiong JiongChen QianZhou Feng