GATA1 (Ab_310) Antibody
- Known as:
- GATA1 (Ab_310) Antibody
- Catalog number:
- E021042-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- GATA1 (Ab_310) Antibody
Ask about this productRelated genes to: GATA1 (Ab_310) 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 (Ab_310) Antibody
Related articles to: GATA1 (Ab_310) Antibody
- 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 - Acute Myeloid Leukemia (AML) is driven by complex interactions between genetic mutations and epigenetic dysregulation. While alterations in chromatin modifiers are frequent, the precise downstream transcriptional networks they enable and how these networks execute the leukemogenic program remain incompletely defined. - Source: PubMed
Publication date: 2026/05/30
Zeng LihuaLei HaohaoBi JingnanRun GuoweiYu BizhenJi Linhua - - Source: PubMed
Bodine David M