ELK3 antibody - middle region (P100856_P050)
- Known as:
- ELK3 (anti-) - middle region (P100856_P050)
- Catalog number:
- p100856_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ELK3 antibody - middle region (P100856_P050)
Related genes to: ELK3 antibody - middle region (P100856_P050)
- Gene:
- ELK3 NIH gene
- Name:
- ETS transcription factor ELK3
- Previous symbol:
- -
- Synonyms:
- ERP, NET, SAP2
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-23
- Date modifiied:
- 2019-01-21
Related products to: ELK3 antibody - middle region (P100856_P050)
Related articles to: ELK3 antibody - middle region (P100856_P050)
- Advances in single-cell and spatial assays have revolutionized the scale and resolution of molecular tissue profiling. Here we present MetaPlaq, a multimodal atlas of human atherosclerotic arterial beds comprising over a million cells across single-cell transcriptomics, epigenomics and high-resolution spatial expression assays. We map granular cell states and disease-relevant transcriptional programs within the native tissue context of coronary arteries. Furthermore, we map cardiovascular GWAS signals to smooth muscle cells (SMCs) and endothelial cells (ECs) and uncover the -regulatory architecture governing their phenotypic transitions. Our comprehensive epigenomic reference allowed us to build cell-specific enhancer-gene link maps and multimodal gene regulatory networks (GRNs) underlying disease-relevant states such as osteogenic SMCs and ECs undergoing mesenchymal transition. We also integrate SMC and EC disease-associated gene sets with GRNs to nominate key transcription factors such as PRRX1, BNC2 and ELK3 regulating atherosclerosis-relevant transcriptional programs. Finally, we layer single-cell and spatial modalities to fine-map GWAS variants with improved cell and anatomical context. We highlight candidate cell-specific regulatory mechanisms at less characterized CAD loci, including and in ECs. Together, this atlas represents an important step towards fully interpreting genetic risk loci and informing new therapeutic strategies for cardiovascular disease. - Source: PubMed
Publication date: 2026/05/26
Mosquera Jose VerdezotoTang IvoryMurach MariaAuguste GaëlleKodali AditiHart PatrickShaw Douglas MLi MinghongTurner Adam WHodonsky Chani JDworak Natalia Mde Oliveira Ana KarinaSol-Church KatiaJhee Teresavan der Sijs Kirsten I MAdkar Shaunak SChoi Ryan BVacante FrancescaWu Joseph CCheng PaulGiannarelli ChiaraLeeper Nicholas JFinn Aloke VBjörkegren Johan L MKovacic Jason CYurdagul Arifvan der Laan Sander WMiller Clint L - Cisplatin resistance remains a major obstacle in the treatment of ovarian cancer (OC). Although ELK3, an ETS transcription factor, has been implicated in chemoresistance across various cancers, its specific role and molecular mechanisms in OC progression and cisplatin resistance remain poorly understood. - Source: PubMed
Publication date: 2026/05/19
Peng QihuaLeung KahoSun YixuanZhang ShiyuTeng YinchengDong Xiaojuan - Multiple myeloma (MM) typically evolves from monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM). Its progression is accompanied by significant tumor heterogeneity and immune microenvironment remodeling, and MM remains largely incurable despite therapeutic advances. Elucidating cellular heterogeneity and regulatory mechanisms involved in disease progression is critical for understanding MM pathogenesis. - Source: PubMed
Publication date: 2026/04/20
Song ChengchengChen TaowuYu SijiaHuang TianjiaoChen TianxinWang CuicuiLiang Yanchen - Left-sided colorectal cancer (LCRC) and right-sided colorectal cancer (RCRC) show marked differences in prognosis and therapeutic response, yet the underlying molecular mechanisms remain poorly understood. We hypothesize that these clinical differences reflect distinct cell-type-specific transcriptional programs and microenvironmental interactions that can be resolved at single-cell resolution. To test this hypothesis, this study analyzed single-cell transcriptomic data from 16 colorectal cancer (CRC) patients (8 LCRC and 8 RCRC), revealing molecular differences between LCRC and RCRC in tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells, and constructing a differential atlas of LCRC versus RCRC. Significant molecular and cellular differences were observed between LCRC and RCRC. was markedly upregulated in RCRC tumor cells and associated with poorer patient survival, potentially regulated by transcription factors , , and . RCRC showed an increased proportion of the CD8-EFFECTOR 3 subpopulation, which co-expresses effector and exhaustion markers, suggesting favorable immunotherapy response. In contrast, the CD4-heat shock proteins (CD4-HSP) subpopulation was almost exclusively present in LCRC, suggesting a potential correlation with a weaker response to immune checkpoint inhibitors. Additionally, ligand-receptor interactions were significantly enhanced in RCRC, potentially contributing to worse prognosis by inhibiting APP protein cleavage and promoting its accumulation. Validation was performed using an independent single-cell transcriptomic dataset, bulk RNA-seq data from TCGA CRC samples, and qPCR on locally collected CRC tissue specimens. In addition, a spatial transcriptomic dataset of CRC and immunohistochemistry data from the Human Protein Atlas (HPA) database were also used to validate part of the findings. This study provides a comprehensive single-cell transcriptomic atlas highlighting the molecular and cellular disparities between LCRC and RCRC, offering novel insights into tumor biology and informing the development of personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/03/17
Zhao ChengzhiZhou WeiyeZeng GuangjianHuang YeenShi ChuanMa HaibeiLi YangLv JiachunLiang XiaohuaFang Shenying - Fat mass and obesity-associated protein (FTO) is a Fe(II)/2-oxoglutarate-dependent RNA demethylase that removes the N6-methyladenosine (m6A) mark and rewires post-transcriptional gene control. In leukemia, FTO is often overexpressed and promotes leukemogenesis by increasing the stability and translation of mRNAs that govern differentiation, metabolism, and survival. In acute myeloid leukemia (AML), FTO-dependent m6A erasure is associated with impaired differentiation (e.g., ASB2/RARA), reinforcement of MYC/CEBPA programs, and glycolytic and stress-adaptation pathways that support therapy resistance and relapse. In acute lymphoblastic leukemia (ALL), FTO contributes to disease maintenance through metabolic rewiring (e.g., ELK3-driven glycolysis), repression of tumor-suppressive transcripts (e.g., IRF8), and stabilization of ribosome-biogenesis mRNAs that sustain proliferative fitness, with additional influence from microenvironmental cues such as exosome-mediated transfer. Preclinical studies show that genetic depletion, small-molecule inhibition, or targeted degradation of FTO increases m6A on key targets, suppresses leukemic growth, and can sensitize cells to standard therapies, supporting FTO as a druggable epitranscriptomic vulnerability. This review summarizes FTO structure and function, highlights subtype-specific mechanisms in AML and ALL, and discusses emerging therapeutic strategies and translational challenges. - Source: PubMed
Publication date: 2026/02/04
Zhang YinliQian Shenxian