Ask about this productRelated genes to: SOX17 antibody
- Gene:
- SOX17 NIH gene
- Name:
- SRY-box 17
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-15
- Date modifiied:
- 2015-11-23
Related products to: SOX17 antibody
Related articles to: SOX17 antibody
- Both rare and common variants in the SRY-Box Transcription Factor 17 ( ) locus are associated with pulmonary arterial hypertension (PAH). SOX17 dysregulation leads to pulmonary artery endothelial cell (PAEC) dysfunction and the obstructive remodelling that characterises PAH. - Source: PubMed
Publication date: 2026/05/18
Vasilaki EleniAkosman BediaSong ShanshanWalters RachelSharma YaminiPereira MandyKeles MerveMykytyuk Nadiya VMaude HannahSingh NavneetField GeorgeVentetuolo Corey EHoward Luke SAman JurjanWilkins Martin RKlinger James RZhao LanCebola InêsLiang Olin DRhodes Christopher J - Combinatorial binding of transcription factors (TFs) is central to eukaryotic gene regulation, providing regulatory specificity and robustness to cell fate control. However, its impact on epigenetic regulation remains poorly understood. Here, we show that the pioneer TFs GATA6, EOMES, and SOX17 cooperate with the zinc finger TF PRDM1 to recruit Polycomb Repressive Complexes (PRCs) and establish enhancers marked by H3K4me1 and PRC-associated histone modifications during endoderm development. Increasing the number and diversity of pioneer TFs bound at enhancers drives synergistic nucleosome remodeling and promotes the formation of "hyper-bivalent" enhancers that reinforce repression of alternative-lineage programs. Together, our findings demonstrate that combinatorial pioneer TF binding creates locally accessible regions that facilitate recruitment of not only active but also PRC-associated epigenetic regulators to preserve lineage fidelity during development. - Source: PubMed
Publication date: 2026/05/21
Mirizio GerardoBuckley MorganLudwig KatieMatsui SatoshiSampson SamuelLim Hee-WoongIwafuchi Makiko - This study investigated the effects of environmentally relevant concentrations of deoxycorticosterone acetate (DOCA) on embryonic development and oxidative stress in zebrafish (Danio rerio), while also elucidating the underlying molecular mechanisms. Embryos were exposed to DOCA at 5, 50, and 500 ng/L, spanning both environmentally pertinent and elevated concentrations. Integrated morphological and transcriptomic analyses (RNA-seq and qRT-PCR) demonstrated dose-dependent acceleration of development, along with alterations in pigmentation, oxidative balance, and metabolic processes. At 50 ng/L, yolk extension increased by 43.3 %, whereas yolk sac area decreased by 3.28 %. At 500 ng/L, these effects intensified (yolk extension: 44.4 %; yolk sac area: -5.28 %). Body pigmentation decreased by 13.7 % compared to controls at 500 ng/L. At 5 ng/L, ROS levels and MDA content increased by 66.5 % and 53.4 %, respectively. Transcriptomic profiling at 16 h post-fertilization in embryos exposed to 500 ng/L DOCA identified significant gene expression changes concordant with phenotypic outcomes: (1) upregulation of six7, sox17, and cdx1a (associated with accelerated development); (2) downregulation of dct and slc45a2 (consistent with reduced pigmentation); (3) altered redox homeostasis, indicated by nox1 upregulation and hemoglobin gene downregulation; and (4) enhanced glycolytic/gluconeogenic activity, evidenced by upregulated pfkfb3, aldob, and pck2. These results demonstrate that the DOCA exposure perturbed embryonic zebrafish development, promoting accelerated morphogenesis concurrent with metabolic alterations and oxidative stress. This study provides the first evidence of DOCA's adverse effects on fish and advances understanding of understudied corticosteroids in ecotoxicology. - Source: PubMed
Publication date: 2025/10/28
Liu ShenaoWang KaifengHuang WenweiZhang JiemingHan ChongLi QiangGong Jian - High levels of DNA damage repair (DDR) can promote the survival, immune evasion, and drug resistance of colorectal cancer (CRC) cells, consequently facilitating the advancement of CRC. This study was designed to investigate the inhibitory effect of berberine (BBR) on CRC progression and the underlying mechanism involving DDR regulation, to provide a novel theoretical basis for clinical CRC treatment. First, we found that BBR demonstrated a dose-dependent inhibition of the viability of CRC cells. BBR promoted apoptosis and suppressed the DDR in CRC cells by upregulating SOX17. Overexpression of SOX17 restrained CRC cell viability and facilitated cell apoptosis. BBR inhibited the DDR of CRC cells by inactivating the β-catenin/TCF4 pathway through the regulation of SOX17. Furthermore, TCF4 transcriptionally activated PIM3 expression. Knockdown of SOX17 partially eliminated the suppressive effects of BBR on CRC cell viability and DDR. Conversely, PIM3 silencing reversed the effects of SOX17 knockdown. In conclusion, we demonstrated BBR inhibits DDR in CRC cells via mediating the SOX17/TCF4/PIM3 axis, thereby blocking CRC progression. This regulatory axis serves as a potential therapeutic target for CRC, and BBR holds promising application prospects as a DDR inhibitor in CRC clinical intervention. - Source: PubMed
Publication date: 2026/05/27
Hu FanWang WeiLi MeiShi QianQue JunjieHuang Pan - Biliary atresia (BA), the leading cause of pediatric liver transplantation, is characterized by neonatal jaundice and progressive extrahepatic bile duct obstruction, yet its pathogenesis remains elusive. To uncover extrahepatic cholangiocyte injury, we generated patient-derived extrahepatic cholangiocyte organoids (EHCOs) from bile duct remnants of BA and controls. We performed discovery bulk RNA-seq followed by targeted molecular and functional validation. Transcriptomic profiling and pathway/perturbation analyses revealed dysregulation of ER stress pathways, xenobiotics/drug metabolism, and genes regulating cell adhesion and polarity. BA EHCOs exhibited altered expression of E-cadherin, RhoU, SOX17, and CFTR. ER stress markers PERK, BiP, and ATF4 were elevated, and TEM demonstrated abnormal ER morphology. Conversely, CHOP, ERO1A, WFS1, and SOD3 were downregulated, suggesting impaired ER stress resolution. Functionally, BA EHCOs were more susceptible to toxic injury, and CYP450 inhibition attenuated ER stress genes expression. Immunostaining of BA liver hilum biopsies confirmed elevated PERK and BiP. Together, these data identify unknown arms of ER stress and epithelial dysfunction as disease-relevant injury process of the extrahepatic biliary tree and potentially implicate xenobiotic metabolism as a modifiable driver. - Source: PubMed
Publication date: 2026/05/07
Har-Zahav AdiHamoudi YaraDanan KerenTobar AnaBespalchik MichalGurevich MichaelShamir RaananGat-Viks IritWaisbourd-Zinman Orith