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
- Hematopoietic stem cells (HSCs) constitute an organized hematopoietic system that undergoes age-related alterations, including increased platelet production and decreased erythropoiesis. The fundamental mechanisms driving these shifts remain incompletely understood. We used single-cell RNA sequencing data to show that old HSCs contain two distinct transcriptional programs: one shared with megakaryocytes and the other reflecting the most primitive HSC state. Developmental time-series profiling further suggests that the acquisition of these programs begins early in life, with the primitive module rising prenatally and megakaryocytic priming emerging after birth. Using a fine-tuned Geneformer (transformer-based deep learning model) to capture higher-order differences between young and old HSCs, coupled with transcriptomic and epigenetic profiling, as well as transcription factor screens, we identified Pbx1 as a key regulator of these age-related transcriptional and differentiation changes. Specifically, Pbx1 suppresses erythroid differentiation by repressing Gata1 expression. These findings provide insight into HSC aging and may inform approaches to modulate age-associated HSC dysfunction. - Source: PubMed
Publication date: 2026/08/21
Kobayashi HiroshiWatanuki ShintaroShiozawa YusukeOshima MotohikoKoide ShuheiTakayama NaoyaMorikawa TakayukiHaraguchi MihoTamaki ShinpeiAsakura TakayoshiMiyata ToshioIwama AtsushiOgawa SeishiTakubo Keiyo - Macrophages are abundant in the tumor microenvironment and contribute to cancer progression through cytokine secretion and intercellular communication. This study combined paired transcriptomic and metabolomic screening with functional analyses to investigate the relationship between hexokinase domain-containing 1 (HKDC1) and macrophage-related responses in hepatocellular carcinoma (HCC). HKDC1 was preferentially detected in an HCC-cell-derived ectosome-enriched fraction under the present isolation conditions. Exposure of THP-1 cells to fractions derived from control HCC cells increased glucose uptake, lactate release, macrophage-associated markers, and an M2-associated gene profile, whereas these effects were attenuated when HKDC1 was silenced in the donor HCC cells. The inhibitory effects of 2-deoxy-d-glucose supported the involvement of recipient-cell glycolytic activity in the observed phenotype. GATA1 contributed to the transcriptional regulation of HKDC1 in HCC cell lines. In addition, HCC-derived extracellular fractions increased CCL1 secretion from THP-1 cells, and CCL1 treatment increased extracellular HKDC1 abundance without a corresponding increase in cellular HKDC1, suggesting a putative feed-forward relationship. HKDC1 was also detected in plasma extracellular-particle-enriched preparations from an HCC mouse model and patients with HCC, and tumor HKDC1 expression was associated with macrophage-related markers and poorer survival. Collectively, these findings support an association between donor-cell HKDC1 and the macrophage-modulating activity of HCC-derived ectosome-enriched fractions. Direct HKDC1 transfer, HKDC1-specific enzymatic activity in recipient cells, and the diagnostic or treatment-predictive utility of circulating HKDC1 remain to be established. - Source: PubMed
Publication date: 2026/08/19
Duan HeqingLiu XiangjunYang XichongCai DechenLi XueqinCao JingzhuLiu JingLiao ShoushengLiu YiyiZou Zhenhong - 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