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)
- Inherited genetic variation substantially increases the risk for developing childhood B-cell acute lymphoblastic leukemia (B-ALL), the most common cancer in children, yet the underlying mechanisms remain poorly understood. To address this limitation, we employ a single-cell multiomic framework to functionally dissect common regulatory variants associated with B-ALL risk. Coupling this multiomic analysis with assessment of allelic skews in chromatin accessibility, we reveal the impact of risk alleles and disruptions in transcription factor networks specific to B-cell progenitors, thereby providing mechanistic insights into altered regulatory programs underlying B-ALL predisposition. By constructing long-range variant-to-target gene maps, we identify 34 high-confidence B-ALL susceptibility genes. Among these, we uncover and functionally validate a risk allele that selectively upregulates expression of , a previously unrecognized regulator of B-cell development and leukemogenesis. Together, these findings establish a comprehensive variant-to-function map of cell state-specific regulatory disruptions underlying inherited predisposition to B-ALL and define new risk mechanisms, which could pave the way for future targeted prevention approaches. - Source: PubMed
Publication date: 2026/08/07
Lee Andrew JNeehus Anna-LenaWahlster LaraAgarwal GauravWeng ChenZhang AllisonLiu TanxinShelton SpencerYe TianyiVolpe Lucrezia DellaCohn OfirPoeschla MichaelKing EmilyHa Samuel ATurvey Alexandra KChiang Charleston W KWiemels Joseph Lde Smith Adam JSankaran Vijay G - Tumorigenesis is a complex multistage process, with its primary regulatory mechanisms involving the interplay of genetic alterations, immune dysfunction and metabolic abnormalities. Transcription factors serve a crucial role in gene expression regulation, participating in various tumor behaviors such as proliferation, metastasis, angiogenesis and drug resistance. Notably, the abnormal activity of transcription factors is closely associated with cancer initiation and progression, and can promote tumor growth, invasion and therapeutic resistance by regulating angiogenesis, epithelial-mesenchymal transition and metastasis-related gene expression. ELK3 belongs to the ETS transcription factor family and the ternary complex factor subfamily. ELK3 participates in multiple molecular biological processes, and is associated with the initiation, progression, invasion and metastasis of various tumors. The present review summarizes the latest research on the structure of ELK3 and its regulation in normal and tumor tissues, focusing on its primary functions in tumors and the signaling pathways involved. Additionally, the diagnostic value of ELK3 as a biomarker and its potential as a target for tumor-specific therapy are explored. - Source: PubMed
Publication date: 2026/07/29
Liu ZhenzheWei ZhongLi ZhenshengZhou Liqiang - BackgroundThe main aim of this study is to identify prognostic biomarkers through integrating bioinformatics analysis in gastric cancer, which is a significant global health challenge.MethodsGene expression datasets related to blood, tissue, and saliva in gastric cancer were downloaded from the Gene Expression Omnibus (GEO) database and analyzed. The bioinformatics approaches included the identification of differentially expressed genes (DEGs) and enrichment analysis, as well as Kaplan-Meier Plotter survival analysis. The DEGs were also validated through The Cancer Genome Atlas (TCGA) database. Additionally, DEGs-associated lncRNAs and microRNAs were identified. Subsequently, Tumor and Immune System Interaction Database (TISIDB) was utilized to examine the correlation of the genes of interest with immune and molecular subtypes.ResultsTwenty-six common DEGs were identified across blood, tissue, and saliva samples. Among them, 17 genes showed significant expression based on TCGA data. RAB23, LOX, ELL2, ELK3, CENPF, CD44, ANP32E, AKR1C2, and SMAD5 displayed significant association with patient survival. Particularly, ELL2 exhibit decreased expression in all specimens. The results indicated that ELL2 has a significant correlation with the immune system. The ELL2 gene regulates immune cell functions in gastric cancer, potentially influencing cancer immune responses, and tumor progression.ConclusionELL2 downregulated expression and its correlation with survival across blood, tissue, and saliva samples using bioinformatics analysis underscores the necessity of more investigation to fully comprehend its function in cancer immunology. - Source: PubMed
Publication date: 2026/06/23
Zare KiarashSalehi ZahraMorovat Ali RezaAghajani AliMohammadi Pour PardisGhanbariasad AliNaghizadeh Mohammad Mehdi - 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