Elk1 EMSA Kit
- Known as:
- Elk1 EMSA Kit
- Catalog number:
- AY1082
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Elk1 EMSA Kit
Related genes to: Elk1 EMSA Kit
- Gene:
- ELK1 NIH gene
- Name:
- ETS transcription factor ELK1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-01-21
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- Non-small cell lung cancer (NSCLC) is characterized by high incidence, mortality, and poor patient prognosis, with chemotherapy resistance being a common challenge. This research intends to identify key molecules involved in NSCLC and elucidate the regulatory role of the LINC01605/miR-7111-5p/ELK1 axis in chemotherapy resistance. LINC01605 and its downstream targets were predicted using the lncRNASNP2-human and miRDB databases. RT-qPCR was employed to measure the expression of LINC01605 across different NSCLC patients, and its prognostic value was assessed through ROC curve, Kaplan-Meier curve, and Cox regression. Dual-luciferase reporter assay was conducted to verify interactions between miR-7111-5p and LINC01605 or ELK1. Transwell assay evaluated cell invasion capabilities, while CCK8 assay confirmed changes in chemotherapy drug sensitivity in chemotherapy-resistant cells across different treatment groups. Elevated expression of LINC01605 was observed in NSCLC patients, correlating with reduced survival rates, and its expression was further elevated in patients with chemotherapy resistance. The upregulation of miR-7111-5p inhibited the proliferation and invasion of NSCLC cells induced by LINC01605. Mechanistically, LINC01605 negatively regulated miR-7111-5p expression while positively influencing ELK1 expression. Silencing ELK1 and upregulating miR-7111-5p levels reversed the chemotherapy resistance of A549 cells induced by LINC01605. By targeting the miR-7111-5p/ELK1 regulatory axis, LINC01605 induced chemotherapy resistance in NSCLC, highlighting its potential as a significant biomarker for NSCLC. - Source: PubMed
Publication date: 2026/05/15
Zhang FangYang Zhi-LiangQin Tian-TianZhang Guo-JunLi Xiang - Postmenopausal Osteoporosis (PMOP) is an age-related disease prevalent among elderly women, characterized by decreased bone density and increased fracture risk. This study investigates the mechanisms of traditional Chinese medicine (TCM) in treating PMOP. - Source: PubMed
Publication date: 2026/05/08
Xiao HefangWang YaobinChen YiGeng BinXia Yayi - Ferroptosis induction is a novel strategy for treating human cancers; however, the detailed mechanisms underlying ferroptosis resistance during nasopharyngeal carcinoma (NPC) progression remain unclear. Herein, we explored the role and potential mechanism of LINC00839 in ferroptosis resistance of NPC cells. We found that the expression levels of LINC00839 and transcription factor ets-like kinase 1 (ELK1) were elevated in NPC tissues, which were associated with a poor survival of NPC patients. Overexpression of LINC00839 or ELK1 reduced the sensitivity of NPC cells to ferroptosis-inducing drugs. Mechanistically, ELK1 directly bound to LINC00839 promoter to contribute to its transcription. Subsequently, LINC00839 destabilized ring finger and CHY zinc finger domain-containing 1 (RCHY1) mRNA through recruitment of up-frameshift 1 (UPF1), and consequently inhibited ubiquitination and degradation of DJ-1 protein. LINC00839 knockdown induced NPC cell ferroptosis, which was neutralized by RCHY1 depletion or DJ-1 overexpression. Knockdown of ELK1 or LINC00839 exerted synergistic roles with Erastin or ferroptosis-inducing chemotherapeutic drug Sorafenib to enhance ferroptosis, thereby delaying tumor growth in vivo. In summary, this study reveals that ELK1-mediated transcription activation of LINC00839 promotes ferroptosis resistance of NPC cells by destabilizing RCHY1 mRNA and subsequent repressing DJ-1 ubiquitination and degradation. These findings provide potential therapeutic targets for overcoming ferroptosis resistance in NPC. - Source: PubMed
Publication date: 2026/05/14
Liu FengLi YuLiu HuaiTang LingFang ShuWenWang XiChen PanWang HuiBao MeiHuaHe BinShengGuo Zhen - In this study, we systematically analyzed the dynamic changes in chromatin accessibility and the transcriptional responses in the spleen of largemouth bass () following infection with iridovirus (LMBV) using the assay for transposase-accessible chromatin with sequencing (ATAC-seq) and transcriptome sequencing (RNA-seq). Based on post-infection survival status, largemouth bass were classified into a resistant group (SR) and a susceptible group (SS). A total of 11,317 differentially accessible regions were identified between the two groups, among which the chromatin accessibility of core promoter regions was entirely increased in the SR group, suggesting that chromatin remodeling in these regions may directly participate in the transcriptional regulation of immune-related genes. Functional enrichment analysis revealed that genes associated with differentially accessible regions were significantly enriched in immune-related pathways such as autophagy, apoptosis, Toll-like receptor signaling, and NOD-like receptor signaling. Motif analysis further identified that transcription factors significantly enriched in the SR group included CTCF and heterodimers composed of multiple members of the ETS and FOX transcription factor families. Through integrative analysis, seven transcription factors (CTCF, Spi1, ETV2::FOXI1, FOXJ2::ELF1, FOXO1::ELK1, SPIC, and FOXO1::ELF1) were found to be significantly enriched in core promoter regions. To further screen for differentially expressed genes directly regulated by chromatin accessibility changes, an overlapping analysis was performed between 629 predicted target genes and 2656 differentially expressed genes (DEGs), resulting in the identification of 71 candidate genes. Among these, three immune-related genes (, , and ) belonging to the ETS and FOX families were identified. This study reveals the dynamic chromatin accessibility landscape of largemouth bass in response to LMBV infection and demonstrates that increased chromatin accessibility in core promoter regions is closely associated with the resistant phenotype. Heterodimers of ETS and FOX family transcription factors may participate in antiviral immune responses by regulating the expression of key immune genes such as , , and , providing potential epigenetic molecular markers for disease resistance breeding in fish. - Source: PubMed
Publication date: 2026/05/05
Sun HuiHua JixiangTao YifanLu SiqiWang WenDong YalunZhang LinbingHe JixiangHe JieQiang Jun - Fetal skeletal muscle development involves coordinated interactions among myogenic, stromal, vascular, and immune compartments, yet the cellular and molecular programs guiding tissue maturation remain incompletely understood. To address this, we generated a high-resolution single-cell atlas of fetal female goat skeletal muscle and performed trajectory analysis, transcription factor activity profiling, and intercellular communication mapping. Unsupervised clustering identified RUNX2 mesenchymal progenitors, fibro-adipogenic progenitors (FAPs), myofibroblasts, endothelial cells, macrophages, differentiating myocytes, and mature skeletal muscle fibers, revealing a heterogeneous ecosystem in which stromal populations support myogenic progression and vascular and immune cells contribute to tissue organization. Pseudotime analysis traced a maturation continuum from differentiation-competent myocytes to contractile fibers, marked by sequential activation of extracellular matrix remodeling, cytoskeletal stabilization, and sarcomere assembly. KEGG and GO enrichment highlighted stage-specific engagement of ErbB, Hedgehog, and Hippo signaling, as well as cell cycle and ubiquitin-mediated proteolysis pathways, linking proliferation, differentiation, and structural maturation. Transcription factor profiling revealed early-stage proliferative and morphogenetically permissive states driven by E2F4/5, HMGA2, and HAND2, transitioning to late-stage differentiation, ECM remodeling, and tissue stabilization orchestrated by CEBPB, CREB3L1, ELK1, and E2F2. Cell-cell communication analysis showed a developmental redistribution of signaling authority, from ECM-driven, progenitor-centered networks to modular, structurally stabilized interactions. These findings define the cellular, transcriptional, and signaling framework orchestrating fetal skeletal muscle maturation. - Source: PubMed
Publication date: 2026/04/29
Han ShiyaoXie ShengcanJiang FenfenZou QianhuiLi TianleWang AhuiWang NanLei ChuzhaoTang Young