ELF4 antibody - N-terminal region (ARP31640_P050)
- Known as:
- ELF4 (anti-) - N-terminal region (ARP31640_P050)
- Catalog number:
- arp31640_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ELF4 antibody - N-terminal region (ARP31640_P050)
Related genes to: ELF4 antibody - N-terminal region (ARP31640_P050)
- Gene:
- ELF4 NIH gene
- Name:
- E74 like ETS transcription factor 4
- Previous symbol:
- -
- Synonyms:
- MEF, ELFR
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2019-04-23
Related products to: ELF4 antibody - N-terminal region (ARP31640_P050)
Related articles to: ELF4 antibody - N-terminal region (ARP31640_P050)
- Excessive macrophage activation is thought to be the primary cause of the cytokine storm that results in severe coronavirus disease 2019 (COVID-19) complications. The underlying mechanisms remain elusive, and more research is needed to find disease-critical genes and develop effective therapies. In this study, we used publicly accessible microarray datasets of cytokine storm in cultured human monocyte-derived macrophages challenged with cytokines, and employed bioinformatics, such as weighted gene co-expression network analysis (WGCNA) and differential expression analysis, to dissect gene expression profiles and identify putative disease-related molecules. Initially, three co-expression modules and related key genes were discovered, which highly correlated to macrophages challenged with cytokines. Then, a preliminary gene expression signature consisting of 203 upregulated and 24 downregulated genes was identified. Next, protein-protein interaction analysis and hub gene identification were used to identify 11 crucial hub genes, namely (), (), (), (), (), (), (), (), (), () and (). Then, the LINCS L1000 characteristic direction signatures search engine (L1000CDS2) was employed for drug repurposing studies. Dasatinib was predicted to be the leading therapeutic compound to perturb the gene signature of cytokine storm in human macrophages. Connectivity Map results suggested that dasatinib may normalize ICAM-1 expression. In addition, the results of molecular docking studies and molecular dynamics simulation revealed that dasatinib may spontaneously interact with ICAM-1 via several key residues and form a relatively stable protein-ligand complex. Overall, this work, based on an analysis of co-expression correlation networks, gene expression signatures and pivotal genes in human macrophages challenged with cytokines, combined with drug repurposing studies, demonstrated that dasatinib may interact with ICAM-1 and could be a potential candidate for cytokine storm. However, due to the limitations of computational approaches, further experimental validation is necessary. - Source: PubMed
Publication date: 2026/03/27
Chen ShaojunWu DapengZheng ZheLuo YiyuanZhang Lihua - - Source: PubMed
Publication date: 2026/01/29
Jia XinyiFang YouhongYu Jindan - Lanzhou lily (), a medicinal and edible plant endemic to China, synthesizes bioactive compounds regulated by diurnal temperature variations (DIFs). family genes, key regulators coordinating endogenous rhythms with external changes, are unexplored in this species. - Source: PubMed
Publication date: 2026/01/07
Ma XiaohuiLi YingGuo XudongMeng LingyuWang YinquanSu JunjiJin Ling - During metastatic spread, tumor cells adapt to evade anchorage-independent cell death by upregulating mitochondrial antioxidant systems. We previously showed that ovarian cancer cells upregulate mitochondrial manganese superoxide dismutase (SOD2) following detachment and multicellular aggregate (MCA) formation. SOD2 scavenges mitochondrial superoxide and manipulates cellular hydrogen peroxide levels, both functions necessary for metastasis. Here, we investigated SOD2's metastatic function by assessing its transcriptomic effects in OVCA433 ovarian cancer cells cultured in low-attachment conditions that induce MCAs, mimicking anchorage-independent states in malignant ascites. SOD2 siRNA-mediated knockdown effects in MCAs were compared to adherent culture conditions. RNA sequencing and pathway analysis revealed that SOD2 lies upstream of pro-metastatic pathways, including PI3K/AKT signaling. Notably, in MCAs, cytokine and immune cell signaling pathways were more significantly enriched following SOD2 knockdown. We previously identified SIRT3 as an important SOD2 activity regulator in MCAs. While SIRT3 knockdown resulted in minor transcriptional changes, we identified that FOXO3 and ELF4 transcription factors, important for stress response and immune regulation, are downregulated by both SIRT3 and SOD2 knockdown. Comparing SOD2 knockdown transcriptional changes to the Cancer Genome Atlas, we found SOD2 expression strongly associates with pro-tumorigenic immune signaling in serous ovarian cancer specimens, including genes identified downstream of SOD2 from our siRNA screen. Moreover, SOD2 expression correlated with signatures related to pro-tumorigenic neutrophil and T-regulatory cell populations. Our data suggest SOD2 positively regulates pro-metastatic pathways, and those identified in MCAs more closely reflect gene expression profiles associated with SOD2 expression in patient tumors. - Source: PubMed
Publication date: 2025/11/12
Elhaw Amal TaherTang Priscilla WKamlapurkar ShriyaAl-Saad SarahSrinivasan SnehaLi DanyangTseng George CStraub Adam CHempel Nadine - Intestinal homeostasis disorders (IHDs), driven by food safety issues, pollution, and drug-resistant pathogens, threaten global health. Key factors in intestinal and metabolic diseases (like IBD, obesity, and liver disease) include barrier dysfunction, gut microbiota imbalance, and excessive immune activation. Transcription factors in intestinal epithelial cells are crucial regulators. ELF4, an ETS family transcription factor, plays vital roles in transcriptional regulation, impacting tumorigenesis, the DNA damage response, and the cell cycle. ELF4 deficiency exacerbates alcoholic liver disease (ALD). Significantly, ELF4 is a novel IFN-I transcription factor with antiviral capabilities. Its regulation of the type I IFN response offers new avenues for developing antiviral and anticancer strategies and managing IFN-induced autoimmune disorders. Thus, ELF4 emerges as a promising target for preventing and treating IHD-related diseases. Mechanistic studies could help identify diets or antimicrobials that activate intestinal ELF4 to combat pathogen/virus-induced intestinal diseases. - Source: PubMed
Publication date: 2025/10/23
Xie LinjiangBai HaixinBai ZiyiFu LvYu Haitao