Ask about this productRelated genes to: GATA1 antibody
- Gene:
- GATA1 NIH gene
- Name:
- GATA binding protein 1
- Previous symbol:
- GF1
- Synonyms:
- ERYF1, NFE1, GATA-1, NF-E1
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: GATA1 antibody
Related articles to: GATA1 antibody
- Depression is associated with complex hippocampal pathology, including disrupted signaling and neuronal damage. In this study, we developed a novel targeted nanoplatform using nucleic acid aptamer-modified astrocyte-derived extracellular vesicles loaded with geniposide (Apt-EVs@GP) to investigate its therapeutic mechanism, with a focus on the GATA binding protein 1 (GATA1)/adrenergic receptor beta 2 (ADRB2) axis in a chronic unpredictable mild stress (CUMS) mouse model. Apt-EVs@GP exhibited excellent biocompatibility and targeted accumulation in the hippocampus. Apt-EVs@GP treatment significantly ameliorated depression-like behaviors, as evidenced by enhanced locomotor activity and reduced immobility in standard behavioral assays. Transcriptomic analysis combined with molecular validation identified a key regulatory mechanism: Apt-EVs@GP suppressed stress-induced upregulation of GATA1, thereby relieving its transcriptional repression of ADRB2. This regulatory interaction was confirmed by chromatin immunoprecipitation and dual-luciferase reporter assays. Restoration of ADRB2 expression led to robust activation of the downstream cAMP/PKA/CREB signaling pathway. Functionally, reprogramming of the GATA1/ADRB2/cAMP axis conferred comprehensive hippocampal protection, including attenuation of neuroinflammation, suppression of neuronal apoptosis, and restoration of synaptic integrity. Our findings demonstrate that Apt-EVs@GP alleviates depression by targeting a novel GATA1/ADRB2 mechanism, highlighting its potential as a promising therapeutic strategy against depression-related hippocampal pathology. - Source: PubMed
Publication date: 2026/06/11
Chen YuWen YuetaoXu DiruHao LeiLiu QinglinKuang JiaZhao WangYang Zhao - Avermectin, a widely used insecticide, has raised widespread concern over its potential toxic risk to non-target organisms. The safety of the nervous system occupies a crucial position in pesticide risk assessment, primarily because it is highly susceptible to interference by external chemicals. Within the nervous system, the blood-brain barrier (BBB) plays an essential role in maintaining system stability and function. The Wnt/β-catenin signaling pathway is known to regulate BBB integrity as well as nervous system development. Morphological observations showed that avermectin exposure caused head edema and intracranial hemorrhage in zebrafish larvae. Meanwhile, analysis of the expression levels of key proteins involved in Wnt/β-catenin signal transduction revealed that avermectin inhibited the expression of Wnt1, Wnt3a and β-catenin, and could specifically bind to Wnt1 and β-catenin proteins, indicating that this compound has the potential to disrupt the signal transduction of this pathway. Furthermore, observation of BBB structure using the Tg(flk1:eGFP; gata1:mCherry) line demonstrated that avermectin disrupted BBB integrity, manifested as blood leakage; in the Tg(flk1:eGFP) line, microinjection of DAPI dye revealed obvious substance leakage; observation of astrocyte development using the Tg(gfap:eGFP) line showed that avermectin impaired astrocyte development. In addition, avermectin could specifically bind to tight junction proteins (Claudin-1, Claudin-5 and Occludin) and inhibit the expression of the corresponding proteins and genes. In all experiments, Wnt/β-catenin signaling pathway modulators were applied, and the results consistently indicated that pathway inhibitors aggravated BBB damage, whereas agonists alleviated the damage. This study confirms that avermectin disrupts the integrity of the BBB in zebrafish larvae, and that the Wnt/β-catenin signaling pathway participates in mediating this injury process. - Source: PubMed
Publication date: 2026/05/19
Wang Wei-GuoDu Lin-JingMa Huan-OuXu Wen-PingTao Li-MingLi ZhongCheng Jia-GaoZhao LiZhang Yang - Enhancers are cis-regulatory elements that drive context-specific gene expression, yet their target genes and modes of action remain largely unresolved. Because most disease-associated variants lie in non-coding regulatory DNA, accurate, cell type-specific enhancer-gene (E-G) mapping is essential for understanding genetic risk. However, current E-G prediction frameworks lack the resolution to capture such context-specific interactions. Massively parallel reporter assays (MPRAs) provide measurements of cis-regulatory activity, but their integration into genome-scale E-G models has been limited. Here, we introduce MPRabc, an MPRA-informed model that improves E-G interaction prediction. MPRabc integrates predicted MPRA activity, sequence-derived regulatory features, epigenomic signals, and three-dimensional chromatin contact maps with clustered regularly interspaced short palindromic repeats-based perturbation training data. Benchmarking against validated regulatory interactions shows that MPRabc outperforms state-of-the-art models. We generated high-resolution E-G networks for K562, HepG2, and human induced pluripotent stem cell (hiPSC) cell lines and applied a graph-based framework to identify regulatory architecture, map trait-associated variants and expression quantitative trait loci, and resolve transcription factor drivers of enhancer activity. Across contexts, we accurately recovered lineage-defining regulatory programs, including GATA1::TAL1 in K562, HNF1A/B in HepG2, and POU factor circuits in hiPSCs. Together, these results establish MPRA-informed modeling as a scalable strategy for decoding enhancer function and linking non-coding variants to gene regulatory mechanisms across cellular contexts. - Source: PubMed
DeGroat WilliamKreimer Anat - Transcription factors are modulated by a precisely coordinated set of conditions, including cell context, target sequences and their accessibility, and co-factor recruitment. Disruption to any of these conditions can dramatically affect transcription factor activity, but quantitatively characterizing the consequences of individual mutations-either in the transcription factors themselves or in their target sequences-has remained a technical challenge. Zambo et al. present an innovation on their native holdup assay that measures DNA-protein binding activity under physiologic or near-physiologic conditions and use mutant GATA1-ATP2B4 binding as an illustrative example. This technique holds promise for uncovering the molecular mechanisms underlying genetically-driven diseases. - Source: PubMed
Publication date: 2026/06/01
Takasaki Kaoru - Eyes are essential sensory organs needed by teleost Atlantic salmon for high visual acuity and survival in both the wild and in aquaculture settings. In this work, we assessed the ocular manifestations of Infectious Salmon Anaemia Virus (ISAV) infection in Atlantic salmon by a cohabitation-mediated infection assay and histological and immunohistochemical approaches. The findings reveal that Atlantic salmon with a systemic ISAV infection displayed ISAV antigen accumulation in specific ocular tissues and significant ocular morphological changes that could compromise visual acuity. Immunohistochemical analyses showed that ISAV-related ocular pathological changes correlate with changes in expression levels and/or spatial localizations of IgM, Sox6, Sox9, collagen type 1, Gata1, and CD10 in specific compartments of the eye. The cornea is likely one of the first ocular tissues to be exposed to the cohabitation-mediated ISAV infection. The ISAV-infected Atlantic salmon showed corneal dysplasia, which correlated with increased corneal stromal ISAV antigen expression, dysregulated IgM, Sox6, and collagen type 1 expression, and an induction of Sox9 expression at the corneal surface. The choroid rete mirabile of ISAV-infected eyes showed a decreased complement of erythrocytes, consistent with anaemia, while Gata1 expression, a key mediator of erythropoiesis, was upregulated compared to non-infected eyes, suggesting a potential erythropoietic compensatory response. These findings provide a basis for further study of ISAV-mediated ocular pathological changes and new insight into the pathogenesis of orthomyxoviruses in the eye. - Source: PubMed
Publication date: 2026/06/01
Mahon EmilyKwabiah Rebecca RParadis HélèneSoto-Dávila Manuel ADuglas SatheesGurung Raja RamParamanathan ThurkaVasquez IgnacioAl-Badoosh ShamsLaw JohnSantander JavierFast Mark DGendron Robert L