FOXG1A antibody - N-terminal region (P100984_T100)
- Known as:
- FOXG1A (anti-) - N-terminal region (P100984_T100)
- Catalog number:
- p100984_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXG1A antibody - N-terminal region (P100984_T100)
Related genes to: FOXG1A antibody - N-terminal region (P100984_T100)
- Gene:
- FOXG1 NIH gene
- Name:
- forkhead box G1
- Previous symbol:
- FKHL2, FOXG1B, FKHL4, FKH2, FKHL1, FOXG1C, FKHL3, FOXG1A
- Synonyms:
- HFK2, QIN, BF1, HFK1, HFK3, HBF-3
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-07
- Date modifiied:
- 2018-05-04
Related products to: FOXG1A antibody - N-terminal region (P100984_T100)
Related articles to: FOXG1A antibody - N-terminal region (P100984_T100)
- Anterior-posterior (AP) spatial regionalization is crucial for central nervous system development. Previous studies suggest that morphogen gradients can induce AP patterning in animal and organoid models. While self-organization in early embryogenesis and neurogenesis has been found using geometrically confined microtissues, spontaneously induced AP patterning has not been reported. Here, we show that circularly micropatterned human pluripotent stem cells self-organize into spatially distinct FOXG1-FOXA1+OTX2+ midbrain-like and HOXB4+ hindbrain/spinal cord-like regions. Notably, the tissue then folds inwardly to form a 3D annular structure, maintaining a distinct boundary between OTX2+ and HOXB4+ zones. The reaction-diffusion of BMP/Noggin plays a key role in the mechanism of AP patterning. Our model is validated by its capability to distinguish the teratogenic effects of valproic acid and isotretinoin. Our work suggests a novel regulatory mechanism for AP patterning and provides a tool for fast screening of teratogens. - Source: PubMed
Publication date: 2026/04/16
Xie TianfaJiang HanBrown Lauren EPak ChangHuiSun Yubing - Neurodevelopment relies on precise coordination across molecular, cellular, and circuit-level processes. Conventional studies into neurodevelopmental gene function are primarily guided by tissue- or cell-type-specific expression patterns and inherent protein properties or domain interactions. Consideration of human disease conditions can greatly enhance our understanding of the mechanics underlying forebrain development. In this review, we demonstrate how to combine these approaches using FOXG1 Syndrome, a rare monogenic neurodevelopmental disorder, as an example. We first summarize the core clinical features of FOXG1 Syndrome, then integrate this information with cellular and behavioral analyses of Foxg1 mutant mouse models to elucidate FOXG1's roles in distinct developmental processes, including telencephalic patterning, progenitor maintenance, neuronal migration and maturation, excitatory-inhibitory balance, and myelination. Moreover, we describe the known molecular mechanisms of FOXG1 action beyond pure transcriptional regulation. Finally, we also demonstrate how the spectrum of FOXG1 variants identified in patients, including gene-dosage changes, protein-truncating variants, missense variants, and chromosomal rearrangements, has enabled targeted functional analyses, each providing unique investigational value. Together, we aim to convey how "bedside-to-bench" directed studies can be utilized to refine classical developmental frameworks, and reveal unanticipated gene functions beyond early development. - Source: PubMed
Publication date: 2026/04/15
O'Shea HollyCollins Hutchinson Meagan LLee Jae WLee Soo-Kyung - Cervical cancer carcinogenesis often exhibits significant heterogeneity, and the molecular mechanisms underlying epithelial cell transformation are not fully understood. - Source: PubMed
Publication date: 2026/04/01
He GuangpingLiang JialiDing ZiyangQu XinyuQiu Junjun - Pacific oysters (Crassostrea gigas) are a major aquaculture species among molluscs worldwide, possessing significant ecological and economic value. The mechanism governing sex determination in oysters remains largely unknown. Fox transcription factors are key regulators of vital biological processes, controlling important functions such as tissue development and reproduction. This study presents a genome-wide identification and characterization of the Fox gene family in C. gigas. Through systematic identification, 16 Fox genes were discovered and classified into 13 subfamilies based on phylogenetic analysis and conservation domain analysis. Transcriptomic profiling revealed that FoxK2 and FoxG1 were significantly upregulated during the resting stage, whereas FoxG1 expression was higher in females and males throughout the active gametogenesis stage (P < 0.05). FoxE1 and FoxL2 exhibited elevated expression profiles during female maturation, whereas FoxO, FoxN4, and FoxK2 showed higher expression profiles during male maturation (P < 0.05). At the spawning stage, FoxE1 and FoxK2 were significantly expressed in females, whereas FoxJ1B and FoxK2 exhibited elevated expression in males (P < 0.05). Our findings indicate sexually dimorphic expression patterns of FoxB1, FoxE1, FoxL2, FoxP1, and FoxC1 and their gonad-specific functions. Our research has significant ecological implications for comprehending the sex determination process and offers fresh insights into the Fox gene regulation mechanisms in bivalves. - Source: PubMed
Publication date: 2026/03/22
Chen SitongLi QiHu BiyangDu Shaojun - Ciprofloxacin (CPFX) is a widely used broad-spectrum fluoroquinolone antibiotic. Although its neurotoxic potential in the mature brain has been recognized, its impact on the developing human nervous system remains largely unexplored. Given that the developing brain exhibits heightened vulnerability to environmental and pharmacological insults, we investigated the developmental neurotoxicity of CPFX using human cortical organoids (hCOs) that recapitulate key features of early cortical development. In this study, chronic low-dose CPFX exposure over two weeks induces significant mitochondrial dysfunction, characterized by excessive ROS production and decreased mitochondrial membrane potential (MMP). These mitochondrial impairments were accompanied by alterations in cortical development and disruptions in GABAergic network formation. Mechanistically, CPFX exposure significantly downregulated Forkhead box G1 (FOXG1) expression in hCOs. Molecular docking simulations suggested an interaction of CPFX with the functional domain of FOXG1. Furthermore, FOXG1 knockdown in primary mouse neurons mimicked CPFX-induced mitochondrial hyperactivity and metabolic dysregulation. Microelectrode array analyses revealed aberrant neuronal firing patterns consistent with an epileptiform phenotype. Importantly, aspirin significantly alleviated CPFX-induced mitochondrial dysfunction, restored ATP and ROS levels, and stabilized neuronal electrophysiological activity in primary neurons, underscoring its potential as a therapeutic intervention. Overall, CPFX induces a broad neuropathological phenotype and impair both mitochondrial function and neurogenesis in hCOs, potentially through a mechanism mediated by FOXG1 disruption. These findings offer novel insights into CPFX-induced neurotoxicity and imply FOXG1 as a promising intervention target. - Source: PubMed
Publication date: 2026/03/25
Liu HaxiaoyuJiang LinhongBu QianSun MinZhao YueHe YumanZhou YuanyiHan ShuangDai YanpingZhang DinwenLi HongchunWang LiangXiao YuzhouQin FengChen YaxingLiu ChunqiQin MengWang HongboTian JingweiZhao YingCen Xiaobo