GATA1 antibody - N-terminal region (P100834_P050)
- Known as:
- GATA1 (anti-) - N-terminal region (P100834_P050)
- Catalog number:
- p100834_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GATA1 antibody - N-terminal region (P100834_P050)
Related genes to: GATA1 antibody - N-terminal region (P100834_P050)
- 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 - N-terminal region (P100834_P050)
Related articles to: GATA1 antibody - N-terminal region (P100834_P050)
- Children with Down syndrome (DS) have an elevated risk of developing myeloid leukemia in DS (ML-DS). In addition to mutations in GATA1, which generate the truncated isoform GATA1-short (GATA1s), ML-DS requires additional somatic gene mutations, most frequently in cohesion and polycomb repressive complex 2 (PRC2) genes. Here, we show that PRC2 insufficiency underlies ML-DS pathogenesis. Transplantation of Gata1s fetal liver cells followed by deletion of the cohesion subunit Stag2 and/or the PRC2 component Ezh2 induced megakaryocyte-biased differentiation and expansion of megakaryocytic progenitors, culminating in lethal myelofibrosis. Mechanistically, loss of Stag2 or Ezh2 reinforced Gata1s-driven reduced chromatin accessibility at erythroid transcription factor target loci in pre-megakaryocyte/erythroid progenitors (pre-MegEs), thereby promoting megakaryocytic skewing. Ezh2 loss attenuated the Gata1s-mediated global elevation of H3K27me3 in pre-MegEs, resulting in derepression of a broad set of PRC2 target genes and establishing a functionally PRC2-insufficient state. Similarly, Stag2 loss induced a moderate but significant degree of PRC2-insufficient state in Gata1s progenitors. Furthermore, chromosome 21-encoded miR-125b blocked megakaryocytic differentiation of Gata1s progenitors lacking either Stag2 or Ezh2 alone, but drove full transformation and expansion of CD150+Sca-1+c-Kit+ leukemic stem cell-like populations only upon concurrent loss of both Stag2 and Ezh2, leading to acute megakaryoblastic leukemia in mice. These findings reveal that cohesin and PRC2 insufficiencies converge on PRC2 dysfunction while exerting distinct epigenetic effects, and synergize with trisomy 21 and GATA1s to remodel the epigenetic landscape, driving progression from a preleukemic state to overt leukemia. - Source: PubMed
Publication date: 2026/04/08
Suzuki YutaroNakajima-Takagi YaekoOshima MotohikoOchi YotaroTsuchiya AkihoKoide ShuheiYokomizo-Nakano TakakoKurosawa ShuheiRizq OlaKon AyanaMiyano SatoruRahmutulla BahityarKaneda AtsushiNakayama ManabuKoseki HaruhikoYu EugeneToki TsutomuIto EtsuroOgawa SeishiIwama Atsushi - Children with Down syndrome have a markedly increased risk of developing myeloid leukemia (ML-DS). Although having an excellent prognosis, 10-20% develop relapsed or refractory disease with poor survival, highlighting the need for new targeted approaches. The pathogenesis of ML-DS is tightly linked to fetal hematopoiesis and mutations in GATA1, generating the truncated GATA1short(s) isoform. We identified Delta-like non-canonical Notch ligand 1 (DLK1) as a direct GATA1s target. DLK1, a paternally imprinted transmembrane protein, is highly expressed in fetal liver CD34⁺ cells but absent in adult hematopoiesis, making it an attractive immunotherapeutic target. Chromatin profiling revealed GATA1s occupancy at a distal enhancer within the DLK1-DIO3 locus, driving aberrant DLK1 upregulation in ML-DS. Functional studies demonstrated that DLK1 is a leukemia dependency, as its genetic ablation impaired proliferation and engraftment, induced apoptosis, and altered Notch and β-catenin signaling. Therapeutically, a DLK1-directed antibody-drug conjugate (DLK1-ADC) induced selective cytotoxicity, abrogated colony formation, and significantly prolonged survival in refractory ML-DS PDX models, achieving durable remissions at higher doses. These findings establish DLK1 as a leukemia-specific vulnerability and provide preclinical proof-of-concept for DLK1-targeted therapies in ML-DS and other leukemias with fetal-like expression programs. - Source: PubMed
Publication date: 2026/04/07
Verboon LonnekeBarwe Sonali PTavenner MeredithFaust Joshua RIssa HasanGoncalves-Dias JoséSchuschel KonstantinBhayadia Rajvan Berkel Patrick HSebastian AimyRies Rhonda EPaczesny SophieMeshinchi SoheilHitzler Johann KPikman YanaKolb E AndersHeckl DirkKlusmann Jan-HenningGopalakrishnapillai Anilkumar - Vascular injury is a major contributor to the development of cardiovascular diseases. Following vascular damage, macrophages migrate to the injury site and, during the later stages of vascular repair, secrete cytokines such as interleukin-10 (IL-10) and transforming growth factor-β1a (TGFB1A), thereby promoting vascular regeneration. Previous studies have demonstrated that macrophage recruitment to sites of tissue injury is mediated by the CXCR4A-CXCL12B signaling axis. In a screening of traditional Chinese medicinal herbs for cardiovascular therapeutic potential, root was identified as a promising source of bioactive compounds capable of enhancing vascular repair through modulation of the CXCR4A-CXCL12B axis. - Source: PubMed
Publication date: 2026/03/19
Zhang LiAn LijuanZhao YanchiLu ZhengHuang JiangtaoTang LinglingLv MengzhuMo DashuangShu Liping - BCR-ABL tyrosine kinase inhibitors (TKIs) effectively treat chronic myeloid leukemia (CML), but drug resistance remains a challenge. Inducing erythroid differentiation in CML cells to enhance their sensitivity to imatinib is a potential approach, but the key regulators are unclear. Imatinib-induced apoptosis and erythroid differentiation in CML cells are distinct processes, suggesting specific genes are involved in differentiation. Analysis of the Gene Expression Omnibus revealed that imatinib highly upregulated dual-specificity phosphatase 21 (DUSP21). A recent study showed that DUSP21 can inhibit cell proliferation. Since cell proliferation decreases during differentiation, we investigated DUSP21's role in CML cell differentiation and TKI sensitivity. Imatinib and ponatinib increased DUSP21 expression in imatinib-sensitive CML cells (K562 and BaF3/p210), whereas only ponatinib did so in imatinib-resistant cells (K562R and BaF3/T315I). DUSP21 overexpression promoted erythroid differentiation, reduced cell viability, and enhanced ponatinib-mediated growth inhibition and apoptosis in these cells. Furthermore, DUSP21 increased the expression of the erythroid transcription factor GATA-1 by activating its promoter. GATA-1 knockdown eliminated DUSP21's effects on erythroid differentiation and ponatinib sensitivity in K562 and K562R cells. Collectively, these findings suggest that DUSP21 acts as a positive regulator of erythroid differentiation in CML cells, and its overexpression sensitizes imatinib-resistant CML cells to ponatinib via GATA-1-mediated erythroid differentiation. - Source: PubMed
Publication date: 2026/03/18
Chen Chih-WeiLin Yuan-FengYeh Yi-YanHuang Nai-KueiHuang Huei-Mei - Chronic kidney disease (CKD) is characterized by persistent renal injury and inflammation. Although S100A12 is associated with inflammatory states, its specific role in regulating neutrophil extracellular trap (NET) formation (NETosis) and contributing to renal pathology in CKD remains poorly understood. This study aimed to identify key diagnostic biomarkers and elucidate the mechanism by which S100A12 mediates NETosis in CKD. METHODS: Integrated bioinformatic analysis was performed on combined datasets (GSE37171, GSE66494, and GSE15072). Differentially expressed genes (DEGs) were screened using WGCNA and three machine learning algorithms (LASSO, SVM-RFE, and Random Forest) to identify hub genes. Immune infiltration was analyzed to assess immune cell proportions. Clinical validation was conducted using peripheral blood samples from 43 CKD patients and 17 healthy controls collected between July 2024 and January 2025. Furthermore, in vitro experiments using dHL-60 cells investigated the impact of S100A12 on NET formation and calcium signaling. RESULTS: We identified 622 DEGs significantly expressed in CKD and enriched in inflammatory regulation. Five hub genes (MMP11, CASR, GATA1, MMP7, and S100A12) were identified, yielding a diagnostic model with high accuracy (AUC = 0.940). Immune infiltration analysis revealed that S100A12 expression was positively correlated with neutrophil infiltration. Experimental validation confirmed significantly elevated levels of S100A12 and NETosis markers (PADI4, MPO, dsDNA, and MPO-DNA complexes) in CKD patients compared to controls. Studies in dHL-60 cells demonstrated that S100A12 overexpression promotes NETosis via calcium overload, a process effectively inhibited by the calcium channel blocker verapamil. CONCLUSIONS: Integrated bioinformatic and experimental analyses identify S100A12 as a robust diagnostic biomarker and a key mediator of NETosis in CKD. Targeting the S100A12-mediated calcium signaling pathway offers a promising future direction for mitigating renal inflammation and injury.. - Source: PubMed
Publication date: 2026/03/21
Zhu HongChang XuejieDu YueZhao XianglingJuan ChenxiaMao YanZhou Enchao