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
- Radiation-induced thrombocytopenia (RIT) is a severe, dose-limiting complication of cancer radiotherapy with limited clinical management options. This study investigated the therapeutic efficacy and molecular mechanism of Diosgenin glucoside (DG), a natural constituent uniquely prioritized through a graph-based deep learning virtual screening pipeline utilizing the directed graph intersection network (DGIN) architecture. - Source: PubMed
Publication date: 2026/09/01
Kong WeijieLi ZhichaoLiu ZhixuanWang LongLuo Jiesi - Runt-related transcription factor 1/acute myeloid leukemia 1 (RUNX1/AML1) is essential for the generation of myeloid progenitor cells and differentiation of megakaryocytes (MKs). During megakaryocyte differentiation and maturation, RUNX1 forms transcriptional complexes with transcription factors such as GATA-1, Ets-1, Fli-1, and NF-E2 to promote platelet production. Disruption of RUNX1 is implicated in hematopoietic neoplasms like familial platelet disorder (FPD/AML), myelodysplastic syndrome (MDS) and acute myeloid leukemia. Here, we review the transcriptional regulation of RUNX1 in megakaryocyte differentiation of normal individuals and myeloid leukemia patients. We also summarize post-translational modifications (PTMs) of RUNX1 and discuss their potential implications for novel RUNX1-directed leukemia therapies. - Source: PubMed
Publication date: 2026/08/24
Xie YanNg IanianLiu YuankaiWang HaitaoYang Qiong - 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