FOXA2 Mouse Monoclonal Antibody
- Known as:
- FOXA2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003170-M11
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXA2 Mouse Monoclonal Antibody
Related genes to: FOXA2 Mouse Monoclonal Antibody
- Gene:
- FOXA2 NIH gene
- Name:
- forkhead box A2
- Previous symbol:
- HNF3B
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2016-10-05
Related products to: FOXA2 Mouse Monoclonal Antibody
Related articles to: FOXA2 Mouse Monoclonal Antibody
- While many studies of developmental control have focused on gene activation, less is known about the extent to which regulatory programs are actively repressed in progenitor cells. We previously showed that trimethylation of histone H3 at lysine 9 (H3K9me3) is a repressive mark that is remodeled on protein-coding genes when endodermal progenitors transition to liver and pancreatic β cell fates. Yet whether H3K9me3 is dynamic at promoters and enhancers has not been determined. Here we find that promoters of liver-specific genes are strongly enriched for H3K9me3 in undifferentiated progenitors, whereas such enrichment is not observed at promoters of more broadly expressed liver genes. We further show that enhancers specific to differentiated tissues-including liver, islet, and cerebral cortex-are strongly enriched for H3K9me3 in their corresponding tissue stem and progenitor cells. In hepatoblasts, H3K9me3 contributes to maintaining the undifferentiated state by restricting FOXA2 and HNF4α from binding to most enhancers, while there remain thousands of H3K9me3-marked enhancers where the factors are not restricted from binding. Our findings illustrate how H3K9me3-mediated heterochromatinization can restrict transcription factor engagement in progenitor cells to prevent inappropriate activation during early development. H3K9me3 at enhancers that allow transcription factor binding may reflect developmental competence. - Source: PubMed
Publication date: 2026/05/04
Ito KenjiDonahue GregKatsuda TakeshiKamimoto KenjiZaret Kenneth S - Due to their high persistence and adverse health effects in humans the use of a number of per- and polyfluoroalkyl substances (PFAS) has been restricted. As a consequence, novel PFAS are increasingly being introduced for industrial applications, although toxicological data are still limited or lacking for many of these compounds. This study examined the molecular mechanisms of action of novel PFAS with a focus on mono- and polyether PFAS with linear or branched structures and either carboxylic acid or sulfonic acid functional groups. Differentiated HepaRG cells, a model of human hepatocytes, were exposed for 24 h to different PFAS congeners at three non-cytotoxic concentrations each. Total RNA was isolated and subjected to whole transcriptome analysis. The study provides transcriptomic data for in total 33 PFAS congeners, for 13 of them for the first time. For most PFAS, the number of differentially expressed genes (DEG) increased in a concentration-dependent manner, whereas five PFAS induced only minor transcriptional changes even at the highest test concentration. Ingenuity Pathway Analysis (IPA) revealed broadly comparable transcriptional responses across all 33 PFAS, indicating convergent molecular effects in HepaRG cells despite marked structural differences among the PFAS congeners. The tested PFAS consistently activated canonical pathways related to fatty acid and lipid metabolism, mainly regulated by the nuclear receptor PPARα, and also affected pathways related to xenobiotic metabolism, partially linked to PXR and CAR signaling. In addition, several PFAS inhibited cholesterol and bile acid biosynthesis pathways. IPA further predicted effects on hepatocyte-relevant upstream regulators such as HNF4A, HNF1A, and FOXA2. Finally, IPA tox-function analysis indicated associations between PFAS-induced transcriptional changes and liver diseases related to cholestasis. - Source: PubMed
Publication date: 2026/05/13
Sprenger HeikeAlker WiebkeRocchi AnnaLeo ChiaraGiglio RosaImmobile Molaro GretaDondero FrancescoBraeuning AlbertBuhrke Thorsten - Prostate cancer resistance to androgen deprivation therapy often involves neuroendocrine transformation. Using single-cell RNA sequencing of transgenic adenocarcinoma of the mouse prostate (TRAMP) mice across pathological stages (early adenocarcinoma to late neuroendocrine prostate cancer [NEPC]), we find an early neuroendocrine-initiating cluster marked by elevated HOXD11, conserved in human NEPC. Genetic suppression of HOXD11 blocks neuroendocrine differentiation and restores androgen receptor (AR) signaling. Mechanistically, HOXD11 directly activates FOXA2 and N-methyl-D-aspartate receptor (NMDAR) subunits (GRIN1/GRIN3A), pathways upregulated in NEPC and linked to poor prognosis. Pharmacological NMDAR inhibition with memantine suppresses NEPC progression preclinically. Notably, a preliminary clinical observation in one evaluable patient with chemotherapy-failed NEPC shows radiographic regression of primary and metastatic lesions after memantine treatment. These findings establish HOXD11 as a driver of neuroendocrine transformation and support further investigation of memantine as a candidate therapeutic strategy for NEPC. - Source: PubMed
Publication date: 2026/05/12
Wu TiangeTan SongMao LikaiZhang RuixinHuang EnyaoWang CanLin HaoWang HuiWang XiaolinChen ShengrongLu HaowenLuo CaichenChen YuruiCheng YifeiXia TianyiYan XiangyuZhu ZiqiYou ZonghaoZhi YunlaiZheng XiejunhaoGao TianShi FanChen ZhanFan CongbinZhong FeiNa RongChen MingTeng Gao-JunZhu YiniLi WenchaoXu Bin - Endometrial receptivity is essential for implantation and pregnancy, yet the role of the mA demethylase FTO remains unclear. We examined epithelial Fto and Wnt signaling during the implantation window using CRISPR/Cas9 Fto knockout mice analyzed at gestational day 4.5 and an Ishikawa and BeWo co-culture model. Histology, TUNEL, Immunofluorescence, mA meRIP-seq, CUT&Tag and qRT-PCR were applied. Fto uteri showed reduced weight, glandular loss, altered Ck18, vimentin and Foxa2, and increased Muc1. Fto deficiency elevated Wnt5b and reduced canonical Wnt/β-catenin activity, coincident with diminished H3K27me3 at the Wnt5b locus. Mechanistically, FTO loss increased mA on SUZ12 mRNA, lowering its stability, weakening PRC2 function and de-repressing WNT5B. Functionally, FTO depletion impaired spheroid adhesion and Wnt signaling, reversible by SUZ12 restoration or WNT5B inhibition. Thus, FTO preserves epithelial integrity and endometrial receptivity by stabilizing SUZ12 mRNA and maintaining H3K27me3 mediated repression of WNT5B, implicating the FTO/SUZ12/WNT5B axis in implantation failure. - Source: PubMed
Publication date: 2026/05/11
Zhang MingGuo FengjiaTan LinlinHu XiujuanLu JiafengLi JinchengXia WenjuanLi HongMeng QingxiaHuang Boxian - Accurate quantification of stem cell-derived dopaminergic neurons is essential for advancing cell therapy strategies in Parkinson's disease (PD). Traditional manual stereological methods, while robust, are time-consuming and subject to interobserver variability, limiting their scalability for preclinical and translational studies. This study presents the development and validation of an artificial intelligence (AI)-assisted physical fractionator workflow for unbiased and efficient quantification of human embryonic stem cell (hESC)-derived ventral midbrain dopaminergic (vmDA) neurons in a Parkinsonian rat model. The workflow integrates convolutional neural networks (U-net and DeepLabv3+) within the Visiopharm platform to automate tissue alignment, graft region identification, and cell segmentation/classification based on triple immunofluorescent labelling (TH, FOXA2, HNA). Human-in-the-loop review ensures quality control and allows for flexible adjustment of immunostaining thresholds. Performance was evaluated using paired datasets: brains from Study A (training, validation, and test set) and Study B (out-of-sample test set from a separate experiment). The AI-assisted workflow demonstrated segmentation and counting accuracy comparable to human experts, with high precision, sensitivity, and high F1 scores for both segmentation and quantification. Results showed no significant differences between AI-assisted and manual quantification of total human cells and vmDA neurons across studies, and the workflow substantially reduced hands-on analysis time from 8 h to 1 h per graft. The investment required for AI model development, annotation, and optimization in the initial phase took several months and is regarded as a one-time infrastructure investment. Additionally, the workflow's design enables adaptability for other cell types by integrating relevant markers. These findings highlight the potential of AI-assisted stereological workflows to accelerate and standardize cell quantification in preclinical research, with potential relevance for translational research settings in cell therapy development. - Source: PubMed
Publication date: 2026/05/09
Overgaard AgneteMolnár KataJurtz Vanessa IsabellLie Maria Elena KliboNyengaard Jens Randel