FOXA2 Mouse Monoclonal Antibody
- Known as:
- FOXA2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003170-M09
- 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
- Alcoholic liver disease (ALD) represents a major risk that threatens human health worldwide and lacks effective therapies. Alcohol-induced inflammation and oxidative stress can trigger and aggravate liver steatosis and promote the development of diseases such as alcoholic liver fibrosis without effective treatment. Bruceine A (BA), a compound extracted from traditional Chinese medicine Brucea javanica, exhibits various activities in multiple diseases. - Source: PubMed
Publication date: 2026/07/22
Chen JiaqiLi LinLi XiaWang WenyuWang RuiYang QiWang ChangyuanFu TingMeng Qiang - Cell surface markers are important tools for quality control (QC) and enrichment of cellular subtypes, such as the dopaminergic (DA) progenitors used for treatment of Parkinson's disease (PD). However, the regional specificity of many published surface markers is not fully known. Here, we identified APCDD1 as a surface marker with high regional selectivity for caudal ventral midbrain DA fate, outperforming the specificity of seven other previously published markers in flow cytometry analysis. APCDD1 expression correlated with key markers of caudal ventral midbrain DA fate, and antibody-based sorting for APCDD1 enabled enrichment of DA progenitors and depletion of non-DA populations. In regionally mixed neural populations, APCDD1-high, but not APCDD1-low cells, yielded full motoric amelioration after grafting in a rat model of PD, and the APCDD1-high cells produced a higher proportion of DA neurons co-expressing ventral midbrain markers FOXA2 and LMX1A. Taken together, APCDD1 is a promising tool for improving the QC and enrichment of clinically applied cell products for PD. - Source: PubMed
Publication date: 2026/07/20
Schörling Alrik LSalvador AlisonRifes PedroHänninen ErnoHolm Nygaard AmalieSingh Rathore GauravNelander JennyRågård Christiansen JosefineMøller Jensen SimoneChristos Niclis JonathanGustafsson EmmaAldrin-Kirk PatrickZhang YuParmar MalinKirkeby Agnete - Olanzapine, an atypical antipsychotic agent, is widely used in treating psychotic disorders, yet its metabolic side effects remain a clinical concern. Emerging evidence suggests that dynamic alterations in histone methylation are implicated in olanzapine-induced hepatic lipid metabolic disorders. PHF2, a JmjC family histone demethylase mediating H3K9me2 demethylation, functions as a transcriptional repressor by regulating downstream targets. To elucidate PHF2's role in this process, we utilized an olanzapine-induced dyslipidemia rat model. ChIP-qPCR analysis demonstrated a significant reduction in dimethylated histone H3 lysine 9 (H3K9me2) on the promoters of lipogenic genes (Fasn, Acc1, Scd1) in the liver, accompanied by elevated nuclear expression of PHF2 in olanzapine-treated rats. Co-immunoprecipitation (Co-IP) assays revealed a physical interaction between PHF2 and ChREBP, a glucose-responsive lipogenic transcription factor. Olanzapine was found to enhance the formation of this complex. Overexpression of PHF2 led to upregulated protein levels of FASN/ACC1 and intracellular lipid accumulation, whereas knockdown of PHF2 using siRNA attenuated these effects. Notably, the upregulation of FASN/ACC1 expression induced by olanzapine was markedly diminished in PHF2-deficient AML12 cells via ChREBP-PHF2-mediated H3K9me2 demethylation. Additionally, olanzapine inhibited the nuclear translocation of FOXA2, a PHF2 transcriptional regulator, thereby augmenting PHF2 expression. These findings uncover a novel epigenetic mechanism underlying olanzapine-induced dyslipidemia, positioning the FOXA2-PHF2-ChREBP axis as a potential therapeutic target through modulation of hepatic histone methylation. - Source: PubMed
Publication date: 2026/07/20
Zhang LiZhao XuChen MeiYingPan ZiweiHu Chang-HuaLiu Xuemei - Islet transplantation is a promising treatment for diabetes, but the shortage of donor islets limits its broad application. Induced pluripotent stem cells (iPSCs) provide an alternative source for generating insulin-producing cells; however, whether the somatic cell origin of human iPSCs influences pancreatic endocrine differentiation remains incompletely defined. In this study, we generated iPSCs from human pancreatic duct cells (HD-iPSCs) and compared their differentiation propensity and functional characteristics with human fibroblast-derived iPSCs (HF-iPSCs) under identical differentiation conditions. HD-iPSC-derived cells showed higher expression of pancreatic endocrine and β-cell-associated markers, including insulin, PDX1, and FOXA2, compared with HF-iPSC-derived cells. Flow cytometric analysis further confirmed a higher proportion of insulin-positive cells in differentiated HD-iPSC-derived cells. Functionally, HD-iPSC-derived cells exhibited greater glucose-stimulated C-peptide secretion than HF-iPSC-derived cells, although their secretory capacity remained lower than that of native human islets. Following transplantation into streptozotocin-induced diabetic mice, HD-iPSC-derived cells reduced blood glucose levels more effectively than HF-iPSC-derived cells, and insulin-positive grafts were detected in vivo. These findings suggest that human pancreatic duct cell-derived iPSCs have enhanced pancreatic endocrine differentiation potential compared with fibroblast-derived iPSCs. Although further maturation and optimization are required, pancreatic duct cells may represent a favorable somatic cell source for generating iPSC-derived insulin-producing cells for diabetes cell therapy. - Source: PubMed
Publication date: 2026/07/18
Lim Sung-BinLee Moon-Kyu - Esophageal squamous cell carcinoma (ESCC) represents a highly lethal malignancy. The FOXA2 was involved in cellular proliferation, differentiation, tumorigenesis, and metastasis. The precise regulatory mechanisms of FOXA2 in ESCC progression remain unclear. - Source: PubMed
Publication date: 2026/07/17
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