FOXA2 Mouse Monoclonal Antibody
- Known as:
- FOXA2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003170-M12
- 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
- During the past decade, emerging studies using electrochemistry and nanoscale imaging have demonstrated that partial exocytotic release is prevailing in neuroendocrine cell models. However, due to complicated structure and culture process, few studies have been carried out using neurons, especially human neurons. Here, dopamine (DA) release from individual vesicles and DA content stored within vesicles were quantified from induced pluripotent stem cell-derived DA neurons with electrochemical techniques. The results indicate that around 61% of the total vesicular DA content is released from these neurons during exocytosis. The vesicular content quantified in DA neurons is significantly higher than that in undifferentiated neural progenitor cells, owing to the increased appearance of dense-core vesicles that are able to store more DA molecules than the clear vesicles. When the neurons are differentiated with BAY-K8644, which stimulates neuronal maturation as well as DA release, the release fraction rises to 91%. The use of BAY-K8644 can be considered as chronic stimulation and leads to similar effects on exocytosis as repetitive stimulation, which triggers short-term plasticity. This study demonstrates partial release in DA transmission in human neurons and provides a link between neuronal maturation and the formation of plasticity. Furthermore, this work suggests that the fraction of release in exocytosis at human neurons may be a factor in determining plasticity. - Source: PubMed
Publication date: 2026/03/23
Gu ChaoyiLork AliciaMajdi SoodabehRabasco StefaniaPeng HuashanNi AnjieErnst CarlEwing Andrew G - Despite decades of biochemical and structural studies of the nucleosome, researchers lack genome-scale methods to determine variability in nucleosome structure along individual chromatin fibres. To address this, here we present Iteratively Defined Lengths of Inaccessibility (IDLI), a computational method that maps the single-molecule co-occupancy of structurally distinct nucleosomes, subnucleosomes and other protein-DNA interactions through long-read single-molecule footprinting. IDLI classifies methylase-inaccessible footprints on individual chromatin fibres into (i) linker-histone-associated nucleosomes; (ii) nucleosomes with focal DNA accessibility along the nucleosome wrap; (iii) unwrapped nucleosomes; and (iv) subnucleosomal species such as hexasomes, tetrasomes and other short DNA protections. Applying IDLI to chromatin from mouse embryonic stem cells, we discover that more than 85% of nucleosomes exhibit intranucleosomally accessible DNA (nucleosome 'distortion'). We observe epigenomic-domain- and expression-level-specific patterns of distortion, including at promoters and mouse satellite repeat sequences. Transcription factor (TF) motif occurrence correlates significantly with distinct types of distortion, and degron experiments provide evidence of direct regulation by TFs. We apply IDLI to in vitro endoderm differentiation in human induced pluripotent stem cells and primary mouse hepatocytes. In both cases, we observe distortion at pioneer TF FOXA2 binding sites, demonstrating that distortion is developmentally encoded and present in vivo. Finally, genetic experiments in mice show that a nucleosome-binding domain of FOXA2 directly affects nucleosome structure in vivo, implicating these protein-nucleosome interactions as direct mediators of distortion. Our work suggests extreme but regulated nucleosome structural variability at the single-molecule level. Furthermore, our approach offers opportunities to model TF binding, nucleosome remodelling and cell-type-specific chromatin regulation across biological contexts. - Source: PubMed
Publication date: 2026/04/29
Yang Marty GRichter Hannah JWang SimaiMcNally Colin PMoore Camille MEmadi AliHarris Nicole EDhillon SimaronMaresca MichelaPan HuiminSaunders HaydenYang RuiqiaoOstrowski Megan SAnderson Erika Cde Wit ElzoMaher Jacquelyn JFan YuhongNarlikar Geeta JNora Elphège PWillenbring HolgerGoodarzi HaniRamani Vijay - Metabolic dysfunction associated fatty liver disease (MAFLD) is a rapidly growing global health burden characterized by hepatic lipid accumulation, insulin resistance, oxidative stress, and inflammation. Phyllanthus niruri (PHYLN) is rich in polyphenols and lignans with known antioxidant and anti-inflammatory properties; however, its therapeutic efficacy is limited by poor bioavailability. This study investigated the protective potential of PHYLN extract loaded into niosomal nanocarriers (PHYLN-NIO) against obesity-induced hepatic steatosis and explored its mechanistic similarity to glucagon-like peptide-1 receptor agonists (GLP-1RAs). Rats were divided into seven groups: control, PHYLN-NIO, HFD, HFD + Semaglutide, HFD + Semaglutide + exendin 9–39, HFD + PHYLN-NIO, and HFD + PHYLN-NIO + exendin 9–39. PHYLN-NIO markedly reduced body weight and body mass index, hepatic steatosis, and inflammation, while enhancing antioxidant status, insulin sensitivity, and lipid profiles. Mechanistically, PHYLN-NIO modulated the lncRNA-MALAT1/miR-206 axis, restored GLP-1/GLP-1R signaling, and downregulated key hepatic lipogenic regulators (LXR-α, SREBP-1c, FASN, ACC-1), while upregulating genes involved in fatty acid oxidation and metabolic homeostasis (FXR, PPAR-α, FOXA2). Notably, co-administration of exendin 9–39 reversed these effects, confirming a GLP-1R-dependent mechanism. These findings suggest that PHYLN-NIO effectively targets MALAT1/miR-206/GLP-1R signaling pathways, demonstrating its potential as a promising nanotherapeutic candidate for MAFLD management. - Source: PubMed
Publication date: 2026/04/27
Khater Safaa IHussein Mohamed M AAbdel-Magied Saydat SLotfy Marwa MKhamis TarekAbdelaziz SaharMostafa MahmoudEl-Shaer Noha OsamaEl-Emam Mahran Mohamed Abd - Prostate cancer, particularly metastatic castration-resistant prostate cancer (mCRPC), presents therapeutic challenges rooted in adaptive lineage plasticity and neuroendocrine transdifferentiation. Conventional genome-based models fail to account for the divergent clinical trajectories observed among tumors that share identical driver mutations. This limitation requires reconceptualizing cancer as a dynamic system in which tumor cells can execute context-dependent molecular programs governed by epigenetic and transcriptional network remodeling. This review critically evaluates three convergent technological pillars reshaping prostate cancer research and clinical care. First, conditional reprogramming (CR) enables the rapid generation of patient-derived models that preserve genomic fidelity, intratumoral heterogeneity, and reversible phenotypic plasticity without genetic manipulation. Second, single-cell and spatial multi-omics approaches have clarified the cellular trajectories underlying luminal-to-neuroendocrine transdifferentiation, identifying a therapeutically actionable intermediate state. They have revealed the hierarchical transcription factor network (FOXA2-NKX2-1-p300/CBP) which orchestrates chromatin remodeling during this lethal transition. Third, physics-informed machine learning and digital twin architectures aim to move beyond correlative risk prediction toward mechanistically sound forecasting of tumor evolution, treatment response, and resistance emergence. We address unresolved challenges in prospective clinical validation, spatial heterogeneity capture, regulatory pathways for functional diagnostics, and the imperative for causal, as opposed to associative, inference from perturbational datasets. The integration of these three domains through closed-loop experimental-computational feedback cycles represents a paradigm shift from reactive to anticipatory precision oncology. - Source: PubMed
Publication date: 2026/04/15
Fadiel AhmedMalpani PunitEichenbaum Kenneth DNaftolin FrederickHassouneh AyaChong GeralynOdunsi Kunle - Adolescent idiopathic scoliosis (AIS) is a complex spinal deformity characterized by three-dimensional curvature of the spine with an unknown etiology. Previous genome-wide association studies have identified a single-nucleotide polymorphism (rs6137473) located downstream of which is significantly associated with female AIS risk. - Source: PubMed
Publication date: 2026/04/22
Moody Edward CWade Emma MMizumoto ShujiMcCallum-Loudeac JeremyWilson Megan J