GATA1 (Phospho_Ser142) Antibody
- Known as:
- GATA1 (Phospho_Ser142) Antibody
- Catalog number:
- E011041-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- GATA1 (Phospho_Ser142) Antibody
Related genes to: GATA1 (Phospho_Ser142) 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 (Phospho_Ser142) Antibody
Related articles to: GATA1 (Phospho_Ser142) Antibody
- In Sub-Saharan Africa, the escalating burden of hypertension converges with persistent malaria endemicity, creating a complex clinical challenge marked by increasing rates of resistance to first-line antihypertensive therapies, particularly angiotensin-converting enzyme inhibitors (ACEIs) and Angiotensin II receptor blockers (ARBs). The molecular mechanisms underpinning this therapeutic failure remain elusive. , a Rho GTPase regulating both cardiovascular function and erythrocyte biology, presents a compelling molecular link between these comorbidities, yet its regulatory architecture in this context is uncharacterized. - Source: PubMed
Publication date: 2026/04/21
Ameke Selassie LouisFosu KwadwoAmenga-Etego LucasSarpong Kwabena Amofa NketiaKwofie Samuel Kojo - Children with Down syndrome have a 150-fold increased risk of developing myeloid leukaemia (ML-DS). Unusually for a childhood leukaemia, ML-DS arises from a preleukaemic state, termed transient abnormal myelopoiesis (TAM), via a conserved sequence of mutations. Here, we examine the relationship between the genetic and transcriptional evolution of ML-DS from natural variation; a rich collection of primary patient samples and foetal tissues with a range of constitutional karyotypes. We distil transcriptional consequences of each genetic step in ML-DS evolution, utilising single-cell mRNA sequencing, complemented by phylogenetic analyses in progressive disease. We find that transcriptional changes induced by the TAM-defining GATA1 mutations are retained in, and account for most of the ML-DS transcriptome. The GATA1 transcriptome pervades all stages of ML-DS, including progressive disease that had undergone genetic evolution. Our approach delineates the transcriptional evolution of ML-DS and provides an analytical blueprint for distiling consequences of mutations within their pathophysiological context. - Source: PubMed
Publication date: 2026/04/23
Trinh Mi KSchuschel KonstantinIssa HasanThomas RebeccaParks ConorOszlanczi AgnesOgbonnah ToochiZhou DiMamanova LiraPrigmore ElenaRobertson Emilia RHodder AngusWenger AnnaAnderson Nathaniel DWhitfield Holly JTreger Taryn DGonçalves-Dias JoséStraathof KarinO'Connor DavidYoung Matthew DJardine LauraAdams StuartKlusmann Jan-HenningBartram JackBehjati Sam - 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