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
- Postpartum depression (PPD) is a common and serious mental disorder after childbirth, imposing a heavy burden on mothers, infants, and families. Abnormalities in the tryptophan-kynurenine (TRP-KYN) metabolic pathway are considered to be involved in its pathogenesis, but the role of quinolinic acid phosphoribosyltransferase (QPRT), a key downstream enzyme in this pathway, remains unclear. This study aims to explore the association between PPD in women undergoing cesarean section and gene polymorphisms, as well as other risk factors for PPD. - Source: PubMed
Zhao ShanshanLin GuoxinLi ZiyuanPing AnqiWang SaiyingDuan Kaiming - Definitive hematopoietic stem cells (HSCs) emerge within intra-aortic hematopoietic cell clusters (IAHCs) located in the dorsal aorta of the aorta-gonad-mesonephros (AGM) region during midgestation in the mouse embryo. Thereafter, HSCs migrate to the fetal liver (FL) and finally settle in the bone marrow (BM). We previously showed that the transcription factor Sox17 is expressed in IAHCs. Overexpression of the Sox17 gene in IAHC cells induces the formation of cell clusters in vitro that resemble IAHCs and retain hematopoietic potential. In addition, a previous report showed that Sox17-transduced hematopoietic stem/progenitor cells (HSPCs) in the BM maintained multipotency. However, whether the ability to form such cell clusters differs among hematopoietic sites has not been fully examined. - Source: PubMed
Publication date: 2026/04/23
Itabashi AyumiYokoi YukiSaito KiyokaTsukahara RyotaMelig GerelAzuma KoyaIizuka NaokiTaga TetsuyaNobuhisa Ikuo - Diabetes mellitus, characterized by β-cell dysfunction and loss, results in impaired insulin secretion and chronic metabolic complications. Mesenchymal stem cells represent a promising source for β-cell regeneration owing to their endodermal differentiation potential. This study optimized the differentiation of human tonsil-derived mesenchymal stem cells (TMSCs) into pancreatic β-like cells through the comparative evaluation of two signaling-based protocols. - Source: PubMed
Publication date: 2026/04/22
Yang JiinKim Ha YeongKim So JeongKim Han Su - Vascular endothelial cell dysfunction leads to the breakdown of endothelial barrier integrity, which contributes to sepsis-induced acute lung injury (ALI). The study investigates the role of Cipepofol in regulating endothelial permeability and inflammation during sepsis using a cecal ligation and puncture (CLP) mouse model and human umbilical vein endothelial cells (HUVECs). Our findings demonstrate that Cipepofol treatment inhibits cytoskeletal stress fiber formation and upregulates junction proteins VE-cadherin, thereby preserving endothelial barrier function. These effects were mediated through the γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1). Cipepofol improved sepsis outcomes, including decreased lung injury, leukocyte infiltration, and vascular permeability. Mechanistically, cipepofol-dependent GABA receptor α1 modulated the expression of dual-specificity phosphatase 1 (DUSP1) in lung tissue and endothelial cells of septic mice. DUSP1 knockdown exacerbated p38 and extracellular signal-regulated kinase (ERK)-MAPK signaling and mitochondrial dysfunction, and abolished the protective effects of Cipepofol against lipopolysaccharide (LPS)-induced mitochondrial oxidative stress. Conversely, genetic or pharmacological inhibition of GABA receptor α1 reversed Cipepofol-mediated suppression of p38/ERK-MAPK signaling and reactive oxygen species (ROS) accumulation, confirming DUSP1 as a key downstream mediator. Together, our study unveils that Cipepofol preserves endothelial integrity by depending on GABA receptor α1 to modulate DUSP1 expression, thereby suppressing p38/ERK-MAPK signaling and mitochondrial dysfunction. These findings highlight a potential therapeutic strategy for sepsis-induced ALI. Abbreviations: ALI, acute lung injury; BALF, bronchoalveolar lavage fluid; BCA, bicinchoninic acid; BSA, bovine serum albumin; CLP, cecal ligation and puncture; CIP, Cipepofol; DAPI, 4',6-diamidino-2-phenylindole; DMEM, Dulbecco's modified Eagle's medium; DUSP1, dual-specificity phosphatase 1; ECGS, endothelial cell growth supplement; ECL, enhanced chemiluminescence; ERK, extracellular signal-regulated kinase; FBS, fetal bovine serum; GABA receptor α1, γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1); GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFP, green fluorescent protein; H&E, hematoxylin and eosin; HRP, horseradish peroxidase; HUVECs, human umbilical vein endothelial cells; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1β; IL-6, interleukin-6; i.p., intraperitoneal; LPS, lipopolysaccharide; LV, lentiviral; MAPK, mitogen-activated protein kinase; MFI, mean fluorescence intensity; MOI, multiplicity of infection; PBS, phosphate-buffered saline; PFA, paraformaldehyde; PTX, Picrotoxin; PVDF, polyvinylidene difluoride; qRT-PCR, quantitative real-time reverse transcription polymerase chain reaction; RIPA, radioimmunoprecipitation assay; ROS, reactive oxygen species; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SEM, standard error of the mean; shRNA, short hairpin RNA; siRNA, small interfering RNA; SOX17, SRY-box transcription factor 17; TBST, Tris-buffered saline with Tween-20; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1; VE-cadherin, vascular endothelial cadherin; W/D, wet-to-dry; ZO-1, zonula occludens-1. - Source: PubMed
Publication date: 2026/04/19
Zhou ShutingHe XudongNi XinzheWang AizhongXu Xiaotao - LKB1 mutations in lung cancer promote an immunosuppressive tumor microenvironment, but the underlying mechanisms remain unknown. Using genetically engineered mouse models and human tumor samples, we demonstrate that LKB1 loss leads to high expression of the cytokine leukemia-inhibitory factor (LIF), which through a cancer cell-autonomous autocrine loop, orchestrates the infiltration of immunosuppressive SiglecFHi neutrophils and Arg1+ interstitial macrophages. Genetic deletion of Lifr, the receptor for LIF, on Lkb1-mutant lung tumors revealed that autocrine LIF signaling induces tumor plasticity and the emergence of a Sox17+ dedifferentiated inflammatory cell state. Antibody-mediated LIF neutralization selectively eliminates the Sox17+ tumor cell state, reduces immunosuppressive myeloid cells, and enhances antitumor T-cell responses. Our study uncovers a novel LKB1-LIF axis driving immune evasion and identifies LIF as a potential therapeutic target in LKB1-mutant lung cancer. This work highlights the interplay between tumor genetics, cellular plasticity, and immune regulation in lung cancer progression. - Source: PubMed
Publication date: 2026/04/20
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