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
- Immune escape is a hallmark of cancers, which affects the efficacy of immunotherapy. Herein, this study analyzed the significance of GATA1/FGL1 in the immune escape of cervical squamous cell carcinoma (CESC) to deepen the understanding of immune escape-associated molecular mechanisms. In silico analysis predicted the correlations of FGL1 with CESC prognosis and CD8 T cell infiltration as well as the relation between FGL1 and GATA1. After FGL1 and/or GATA1 gain- and loss-of-function, CC cells were co-cultured with CD8 T cells. The sensitivity of CC cells to CD8 T cells was assessed, as well as the secretion of perforin, GzmB, IFN-γ, and TNF-α. Also, CD8 T cell proliferation and apoptosis were measured. The binding of GATA1 to the FGL1 promoter was validated through luciferase and ChIP assays. GATA1-knockdown U14 cells were transplanted into immunocompetent C57BL/6 mice in combination with or without CD8α mAb to ascertain the impacts of GATA1 on tumor growth and immune escape in CESC in vivo. Knockdown of either FGL1 or GATA1 markedly enhanced the sensitivity of CC cells to CD8 T cell‑mediated cytotoxicity and increased the secretion of perforin, GzmB, IFN‑γ, and TNF‑α. It also promoted CD8 T cell proliferation while reducing their apoptosis. These effects of GATA1 knockdown were partially negated by FGL1. In vivo, GATA1 knockdown prominently diminished the tumor growth and increased the infiltration and cytotoxic effects of CD8 T cells. Collectively, GATA1 knockdown facilitates CD8 T cell responses and suppresses immune escape in CESC by downregulating FGL1. - Source: PubMed
Publication date: 2026/08/13
Zhou JuanLiu FangGao TingtingYang Ying - Myelodysplastic neoplasms (MDS) are a group of heterogeneous clonal hematopoietic disorders with a high risk of progression to acute myeloid leukemia. Despite folic acid being an essential vitamin for human development that can be harmful at high levels, it is still unclear how its excess precisely impacts erythropoiesis in MDS patients. Based on non-targeted metabolomics, we identified significantly elevated folic acid levels in both MDS mice and MDS patients. Functional studies revealed that an excess folic acid diet exacerbated anemia in MDS mice, while restricted folic acid intake alleviated disease phenotypes. Mechanistically, excess folic acid promotes the nuclear translocation of FOLR2, which functions as a transcription factor to bind the promoter of IRF2BP2 and drive its expression. Upregulated IRF2BP2 subsequently represses key erythroid transcription factors GATA1 and KLF1, leading to erythroid differentiation arrest. The folic acid-FOLR2-IRF2BP2 axis is upregulated, and high IRF2BP2 expression correlates with poor prognosis in MDS patients. Our study unveils a novel pathological role of folic acid in promoting MDS progression by disrupting hematopoietic stem/progenitor cells and impairing erythropoiesis, suggesting dietary folic acid restriction and targeting FOLR2-IRF2BP2 axis as potential therapeutic strategies. The FOLR2-IRF2BP2 Axis Mediates Erythropoiesis Impairment by Excess Folic Acid in Myelodysplastic Syndromes. In NUP98-HOXD13 transgenic/MDS mice, folic acid content was significantly increased. Excess folic acid diet exacerbated disease symptoms in MDS mice. Reducing folic acid intake significantly alleviated MDS symptoms. Mechanistically, excess folic acid not only promoted the expansion of hematopoietic stem progenitor cells but also disrupted erythropoiesis involving the FOLR2-IRF2BP2 pathway. - Source: PubMed
Publication date: 2026/08/10
Yang ChaoyingWang YanpengPeng YuanliangWang ZeyuanGuo ZhimingXiao XiaojuanLi HaoboGong HanHu BinLiu LiFu MinCao PengfeiYang XiongbingLiu JingNie LingHan XuZhang Ji - Down syndrome (DS) confers a developmentally rooted predisposition to both myeloid and lymphoid leukemias, particularly myeloid leukemia associated with DS (ML-DS) and acute lymphoblastic leukemia associated with DS (ALL-DS). While trisomy 21-driven gene dosage imbalance is central to this risk, DS leukemogenesis cannot be fully explained by recurrent mutations alone; it reflects a dynamic interplay between altered hematopoietic development, cell-intrinsic programs, and tissue microenvironmental cues. In this perspective, we argue that the field should move beyond cataloging cellular heterogeneity and adopt a topographic, multi-omic framework of DS leukemogenesis. We discuss how fetal niche biology shapes pre-leukemic evolution in ML-DS, including the developmental context of GATA1-mutant clones, and how therapy-driven bottlenecks may promote persistence of spatially protected residual disease in ALL-DS. We further highlight the translational potential of integrating spatially resolved transcriptomics with single-cell and protein-aware multi-omics to identify compartment-specific signaling programs and clinically actionable vulnerabilities. A spatially informed model of DS leukemia may improve biological stratification, clarify mechanisms of relapse and toxicity, and support the development of more effective and less toxic therapeutic strategies. - Source: PubMed
Publication date: 2026/08/06
Peroni EdoardoAmato RosarioBado MartinaFavarato MosèRosato Antonio - Transcriptional activation of cell-type-specific genes is achieved by multiple mechanisms that guarantee chromatin accessibility at -regulatory elements and the long-range interactions between them. Generally, DNA methylation counteracts these processes and promotes gene silencing in vertebrates. CTCF is a conserved and essential multifunctional transcription factor relevant for establishing and maintaining chromatin architecture and accessibility, while its precise role in regulating DNA methylation remains to be determined. We focused on the highly abundant and previously studied erythroid-specific α gene () to systematically investigate the role of CTCF binding on DNA methylation, chromatin accessibility, and gene expression using a chicken erythroid cell differentiation system. The perturbation of CTCF binding at the intergenic region between the embryonic π and the adult α gene resulted in DNA methylation propagation towards the α gene, which was accompanied by decreased chromatin accessibility, GATA-1 binding, and gene expression. Notably, chromatin conformation analyses revealed that CTCF binding enables α transcriptional activation independently of its architectural function. We observed a similar role of CTCF on DNA methylation and gene expression in the human orthologous gene . Our findings support a conserved role of CTCF in preventing DNA methylation spreading and gene silencing of cell-type-specific genes along differentiation. - Source: PubMed
Publication date: 2026/08/03
Tapia-Urzúa GustavoNúñez-Martínez Hober NelsonGarza-Manero SylviaFranke MartinPeralta-Alvarez Carlos AlbertoCerecedo-Castillo Ángel JosuéGuerrero GeorginaGómez-Skarmeta José LuisRecillas-Targa Félix - Vein occlusion (VO), including deep venous thrombosis (DVT) and retinal vein occlusion (RVO), is a common cause of multiple diseases that severely compromise the quality of life of affected individuals. Epidemiological evidence indicates that VO prevalence increases in cold seasons, yet the underlying mechanism remains unknown. Here, we show that cold exposure markedly elevates peripheral platelet counts, thereby aggravating VO in mouse models. Cold-augmented thrombocytopoiesis depends on the activation of adipose thermogenesis and subsequent increase in circulating free fatty acid (FFA) levels. Mechanistically, FFA-β-oxidation promotes acetyl-CoA production, which upregulates and stabilizes C/EBPα by shifting the balance between p300 acetyltransferase and SIRT1 deacetylase. Acetyl-C/EBPα transcriptionally upregulates GATA-1 and NF-E2 for megakaryocyte maturation and platelet production. Depletion of adipose triglyceride lipase PNPLA2, megakaryocyte-specific knockout of key β-oxidation enzyme CPT1α, or pharmacological inhibition of CPT1α and p300 abolishes cold-augmented thrombocytopoiesis and alleviates DVT and RVO in mouse models. In healthy volunteers, tolerable cold exposure activates adipose thermogenesis, increases circulating FFA levels, and increases platelet counts. Moreover, a retrospective cohort study of 425 patients reveals elevated platelet counts and higher DVT incidence during cold seasons. Similarly, increased platelet counts are observed in 448 patients with RVO at the time of diagnosis in cold seasons. Our study provides novel mechanistic insights into the increased VO risk induced by cold exposure and proposes a new therapeutic paradigm for VO by targeting megakaryocyte metabolism. - Source: PubMed
Publication date: 2026/07/30
Xie SisiChen KaihongSun XiaotingYe YingChen RuiboJiang ChenyuChen MingjiaLv XueLi HuilanLiao YingChen WeihuaDeng LinCai LinliLiang YuWei QiaolingZuo JiYu GuohuaYang LiboJi JiansongLin LiTao WeiZhao ChenYang YunlongCao Yihai