GATA2 pSer401 antibody Ab
- Known as:
- GATA2 pSer401 (anti-) Antibody
- Catalog number:
- 1488067
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- GATA2 pSer401 antibody
Related genes to: GATA2 pSer401 antibody Ab
- Gene:
- GATA2 NIH gene
- Name:
- GATA binding protein 2
- Previous symbol:
- -
- Synonyms:
- NFE1B
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2019-04-23
Related products to: GATA2 pSer401 antibody Ab
Related articles to: GATA2 pSer401 antibody Ab
- Tumor-infiltrating clonal hematopoiesis (TI-CH) indicates the infiltration of somatically mutated hematopoietic cells into the tumor microenvironment. While clonal hematopoiesis is a known prognostic factor in hematologic malignant neoplasms, the clinical relevance of TI-CH in solid tumors remains poorly understood. - Source: PubMed
Publication date: 2026/05/07
Yun DabinChen ChengQin NaWang ZhaomingSong Nan - MECOM is a transcription factor critical for the maintenance of hematopoietic stem cells (HSCs) and the pathogenesis of myeloid leukemia. Germline mutations clustered in the C-terminal zinc finger domain (ZFD) of MECOM are known to cause MECOM-associated syndromes, involving bone marrow failure and skeletal anomalies. However, the molecular consequences of these mutations and the precise downstream mechanisms of MECOM remain elusive. Here, we demonstrate that the C-terminal ZFD serves as the dominant DNA-binding module of MECOM, and that disease-associated mutations abrogate its DNA-binding capacity. Mechanistically, we reveal that MECOM functionally antagonizes GATA2 via C-terminal ZFD-mediated DNA binding and recruitment of the corepressor CtBP. This repression promotes myeloid leukemogenesis while suppressing mast cell differentiation. Furthermore, we generated a knockin mouse model harboring a C-terminal ZFD mutation, which successfully recapitulated the clinical phenotypes of MECOM-associated syndromes, including reduction of HSCs and B cells. Collectively, our findings define C-terminal ZFD mutations as loss-of-function mutations with impaired DNA binding, uncover the MECOM-GATA2 axis as a key regulatory pathway, and provide a valuable mouse model for understanding MECOM-associated syndromes. - Source: PubMed
Publication date: 2026/05/05
Iida KoheiNakanishi MayukoNakahara JakushinAsada ShuheiIsobe TomoyaYabushita TomohiroFukushima TsuyoshiTanaka YosukeOzawa ManabuYamada YasuhiroKitamura ToshioYamamoto KeitaGoyama Susumu - Inborn errors of immunity (IEIs) encompass a heterogeneous group of more than 550 genetic conditions with variable ages of onset. A significant proportion of IEI arises from genetic variants that may not yet be fully elucidated or recorded in existing genomic databases. Molecular diagnoses are achieved in approximately 15-35% of IEI cases, yet in only 9-20% of individuals with predominant antibody deficiencies, particularly in adult cohorts. We aimed to evaluate whole genome sequencing (WGS) diagnostic yield in adults suspected to have IEI. Clinical assessments of the patients were carried out at tertiary medical institutions in Timisoara and Bucharest, Romania. The study cohort included a consecutive series of 21 adult patients (aged 19-60 years) with IEI phenotype, who underwent genetic analysis, using WGS as the first diagnostic approach. A definitive molecular diagnosis was confirmed in only 9.5% (2/21) of the participants, in and genes. Variants of uncertain significance (VUS) were detected in three patients (13.6%) in , , genes. For about half of the cohort the onset of the disease was noted in childhood. WGS as a first-line diagnostic strategy in a cohort of adults with IEI yielded a low diagnostic rate. There were significant delays in genetic diagnosis, as half of the cohort experienced childhood-onset symptoms. Results suggest that adult IEI diagnosis remains challenging, necessitating functional studies and longitudinal re-evaluation of genomic data. - Source: PubMed
Publication date: 2026/04/10
Pantea Cristina-LoredanaBataneant MihaelaJurcut CiprianCochino AlexisIoan AndreeaMunteanu Catalin VasileZimbru Cristian GUrtila PatriciaChirita-Emandi Adela - Generation of megakaryocytes (MKs) from stem cells in vitro to produce platelets (PLTs) is an appealing approach for providing an alternative source of PLTs. Understanding the transcriptomic characteristics of MKs in vitro is crucial for providing a theoretical foundation for producing functional MKs more efficiently in the future. - Source: PubMed
Publication date: 2026/05/02
He YanminLiang YueHe JiShen YuWu ZhipanPei ShanshanZhu Faming - Androgen receptor (AR) signaling is central to prostate cancer progression, yet resistance to AR-targeted therapies remains a major clinical challenge. Understanding the molecular consequences of AR pathway inhibition is therefore essential for improving therapeutic outcomes. Here, we identify a previously unrecognized link between AR antagonism and cuproptosis, a copper-dependent form of regulated cell death. Using integrated genomic profiling, we find that AR-targeted agents transcriptionally activate the key cuproptosis regulator Ferredoxin-1 (FDX1), thereby rendering prostate cancer cells markedly more susceptible to copper-induced lethality. Mechanistically, ligand-bound AR directly engages cis-regulatory elements, which are rendered accessible by the pioneer factor GATA2, and drives upregulation upon AR antagonist exposure. Consistent with this mechanism, FDX1 expression is elevated in clinical prostate cancer samples following androgen deprivation therapy or AR antagonist treatment. Increased FDX1 enhances intracellular Cu accumulation, destabilizes Fe-S cluster proteins, and disrupts mitochondrial metabolism, establishing a procuproptotic state. Functionally, combining AR antagonists with copper ionophores synergistically induces cuproptosis and potently suppresses tumor growth in AR-positive prostate cancer cells, three-dimensional (3D) spheroids, patient-derived organoids, and xenograft models, with minimal systemic toxicity. This synergy is abolished by FDX1 loss or copper chelation, confirming dependence on AR-FDX1 axis activation. Together, these findings uncover FDX1 as a mechanistic effector of AR pathway inhibition and propose a well-tolerated combination strategy that exploits cuproptosis to improve therapeutic responses in prostate cancer. - Source: PubMed
Publication date: 2026/05/01
Li XuehuiWang SiliangWei YuangXie ChuangChen YanhuaWu FanchenZhou QianqianSong XiaowenXu XinyiXu DongliangXu LingfanLin ShanYuan Fuwen