CBFA2T3 antibody - N-terminal region (ARP33993_P050)
- Known as:
- CBFA2T3 (anti-) - N-terminal region (ARP33993_P050)
- Catalog number:
- arp33993_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CBFA2T3 antibody - N-terminal region (ARP33993_P050)
Related genes to: CBFA2T3 antibody - N-terminal region (ARP33993_P050)
- Gene:
- CBFA2T3 NIH gene
- Name:
- CBFA2/RUNX1 translocation partner 3
- Previous symbol:
- -
- Synonyms:
- MTGR2, ZMYND4, MTG16, RUNX1T3, ETO2
- Chromosome:
- 16q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-13
- Date modifiied:
- 2016-10-05
Related products to: CBFA2T3 antibody - N-terminal region (ARP33993_P050)
Related articles to: CBFA2T3 antibody - N-terminal region (ARP33993_P050)
- Age-related structural and functional remodeling of the heart and vessels increases cardiovascular disease (CVD) risk, yet comprehensive assessments using multimodal imaging and genetic characterization remains limited. We aimed to quantify cardiovascular aging using multimodal biomarkers and evaluate its genetic architecture, lifestyle determinants, and prognostic relevance. - Source: PubMed
Publication date: 2026/07/30
Abula AdilaYuan YuxinLi XiaoyuZhao YunfengHuang YushuZhang ShengkuiLi ZilinWang Jian'anWu XifengLi Wenyuan - In this paper, we discuss how Nanopore whole genome sequencing (WGS) was utilized for rapid genomic identification of CBFA2T3::GLIS2-rearranged acute myeloid leukemia (AML) for two pediatric patients. Patients with CBFA2T3::GLIS2 AML have a 27% 5-year event-free survival. Prior case reports demonstrated that recurrent CBFA2T3::GLIS2 AML has a favorable treatment response to azacitidine, venetoclax, and gemtuzumab. Nanopore WGS enabled early recognition of the CBFA2T3::GLIS2 rearrangement, providing the opportunity to choose alternative therapies upfront with azacitidine, venetoclax, and gemtuzumab. We discuss our patients' status and the implications of a rapid molecular diagnostic method like Nanopore WGS. Trial Registration: Clinicaltrials.gov identifier: NCT06609928. - Source: PubMed
Publication date: 2026/07/25
Alfred Joanne CGeyer Julie KRodriguez AlexaRoata CorneliaBuddenbaum JessicaThompson Patrick AWang Jeremy RAlexander Thomas B - DNA methylation is an epigenetic mechanism that regulates gene function and plays a crucial role in adaptability traits. Unlike commercial chickens, which have been bred for uniform production performance, desi chickens experience varying environmental pressures, shaping their genetic diversity and survival strategies through organized methylation patterns. We compared global DNA methylation profiles between indigenous (Al, Kn, Nb, and Nn) and commercial chickens (Br and Ly) to identify epigenetic factors. In this study, a single cytosine base modification was observed globally in all six breeds, ranging from 11,935,490 to 44,572,168. Each indigenous and commercial chicken breed exhibited a unique methylation pattern. Further analysis revealed that more than 6979 differentially methylated regions (DMRs) were identified in each indigenous breed compared to the commercial layer and broiler. The identified DMR-associated genes (DMGs) revealed various adaptational processes in each breed. The chicken breeds studied showed different levels of methylation across various genes, indicating breed-specific differences. They were inferred as epigenetic markers for traits, which makes them differ between the breeds, like cognitive behavioral (LINGO1, EFNB1 and NFIA), feed intake (CUX1), thermal stress adaptation (CDC37 and ELOVL5), egg production (RUNX1, and CBFA2T3), hyperpigmentation (SLC31A1), osmotic stress adaptation (SIK1 and Rasd1), growth and carcass quality (LINGO1, PTK7, GPHN, LDB2 and FGF14) and feathering pattern (EFNB1). This study extends our understanding of the epigenetic regulatory mechanisms across different chicken breeds and highlights the value of the environmental adaptability of indigenous germplasm. Finally, we suggest that validating these markers by integrating transcriptomic, phenotypic, and ecological data will be critical for the comprehensive integration of epigenetic and phenotypic data into breeding and conservation biology. - Source: PubMed
Publication date: 2026/07/02
Muthusamy MalarmathiPeters Sunday OAkinsola Oludayo MichaelBalasubramanian Raghavendran VKannan Thiruvenkadan ARekaya RomdhaneAggrey Samuel E - Zinc finger proteins (ZNFs), characterized by zinc ion-binding domains, participate in cell proliferation, differentiation, and metastasis in lung adenocarcinoma (LUAD). However, associations between ZNFs-related genes and clinical outcomes, immune cell infiltration, and immunotherapy remain unclear. To explore feasibility of using ZNFs-related genes as prognostic tools for LUAD risk stratification. Retrospective analyses were conducted utilizing data from TCGA and GSE26939. After screening differentially expressed ZNFs, regression analyses were performed to construct prognostic signature. Enrichment analysis identified biological processes and pathways involved in signature genes, while immune landscape was examined by multiple algorithms. The drug sensitivity analysis identified potential candidate drugs related to the signature genes. Cell experiments indicated the function of the key risk gene CTCFL in promoting the malignant behavior of LUAD cells. A prognostic signature comprising 12 ZNFs-related genes (CBFA2T3, CTCFL, GFI1B, IGF2BP1, RIMS2, TRIM29, TRIML2, ZIC2, ZNF208, KLF10, ZNF750, and ZNF257) stratified LUAD patients into two risk groups, demonstrating robust performance in predicting clinical outcomes. These genes were significantly enriched in epidermal development, intermediate filament cytoskeleton, endopeptidase inhibitor activity, hormone activity, and neuroactive ligand-receptor interactions. Low-risk patients exhibited higher levels of immune cell infiltration (e.g., DCs, B cells, and neutrophils) and superior responses to immunotherapy (anti-CTLA-4 and PD-1/CTLA-4 dual blockade). Possible therapeutic compounds for LUAD patients included SHP-099, Dimethylfasudil, EMD-534085, and PF-2771. The expression of CTCFL enhanced the malignant cellular behavior in LUAD. ZNFs-related gene signature provides predictive insights into LUAD patient survival, immune cell infiltration, and immune checkpoint blockade therapy, serving as a valuable tool to guide clinical decision-making. - Source: PubMed
Publication date: 2026/06/26
Zou MiZheng GuangdaBao Yanju - Sickle cell anemia (SCA) is a condition caused by a mutation in the HBB gene, leading to the production of hemoglobin S in red blood cells. Hydroxyurea (HU), used in treatment, increases fetal hemoglobin (HbF) levels, thereby reducing erythrocyte sickling, as do single-nucleotide polymorphisms (SNPs) in the BCL11A gene and the HBS1L-MYB intergenic region. In this study, we investigated the combined effects of HU therapy, β-globin haplotypes, and SNPs in BCL11A and the HBS1L-MYB intergenic region on HbF levels in a cohort from Western Bahia, Brazil. - Source: PubMed
Publication date: 2026/06/23
de Magalhães Filho Manoel FerreiraSantana Ilana Luize Rochada Silva Pâmela Lourdes PereiraVenancio Larissa Paola Rodrigues