EGR1 EMSA Probe Set
- Known as:
- EGR1 EMSA Probe Set
- Catalog number:
- AY1303P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- EGR1 EMSA Probe Set
Related genes to: EGR1 EMSA Probe Set
- Gene:
- EGR1 NIH gene
- Name:
- early growth response 1
- Previous symbol:
- -
- Synonyms:
- TIS8, G0S30, NGFI-A, KROX-24, ZIF-268, AT225, ZNF225
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-11
- Date modifiied:
- 2016-10-05
Related products to: EGR1 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: EGR1 EMSA Probe Set
- It is well-known that the morbidity and clinical burden of type 2 diabetes mellitus (T2DM) are predominantly associated with its chronic complications, in which fibrosis is a significant contributor. Recently, sodium-glucose cotransporter 2 (SGLT2) inhibitors have made a pivotal advancement in the therapeutic landscape not only improving glycemic control, but also demonstrating high effectiveness in the prevention and treatment of T2DM complications. In this work, we aimed to assess the transcription factors (TFs) mediating the effects of SGLT2 inhibitor empagliflozin (EMPA) treatment by a comprehensive analysis of the allele-specific expression (ASE) events utilizing the RNA-seq data. Initial logistic regression analysis of the in vitro transcriptomic data for EMPA-treated peripheral blood mononuclear cells (PBMCs) of three healthy donors revealed a significant inter-individual variation in ASE for 240 genes linked to EMPA treatment beyond the glucose-lowering effects. Then, 146 TFs were predicted to regulate the expression of the corresponding targets using motifbreakR and DESeq2. Among these, multiple TFs (including ATF3, ATF4, E2F1, EGR1, FOS, JUN, JUNB, IRF8, KLF6, KLF11, SNAI1, TWIST1, and ZEB1) were involved in the TGF-β/SMAD3 canonical profibrotic signaling cascade, pertinent to diabetes-related fibrosis, playing a significant role in the development of diabetic complications. Further analysis of the in vivo data for the PBMCs from ten T2DM patients initiating EMPA therapy identified 98 TFs related to the ASE variation in both in vitro and in vivo cohorts. To conclude, our integrative allele-specific approach enables the prediction of novel EMPA-responsive regulatory interactions and suggests the important mediators of the mechanisms underlying the effects of EMPA on human PBMCs. - Source: PubMed
Publication date: 2026/08/12
Korbolina Elena EGubina MariaBryzgalov Leonid ODegtyareva Arina OEvseenko Anastasia AAntonseva Elena VKorbut Anton IRykova Elena YKlimontov Vadim VKzhyshkowska Julia GMerkulova Tatiana I - Osteoarthritis (OA) is a prevalent degenerative joint disease with a complex molecular basis. This study aims to identify key molecules involved in OA pathogenesis, focusing on the role of acetylation-related gene expression. Public microarray datasets GSE82107 and GSE169077 were integrated to construct a differential expression landscape between OA patients and healthy controls. Acetylation-linked differentially expressed genes (acetylation-DEGs, ARDEGs) were extracted by intersecting DEGs with a curated set of acetyltransferases, deacetylases and acetylation substrates. A protein-protein interaction (PPI) network was built and subjected to LASSO-penalized regression to prioritise hub genes. Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG) and Gene Set Variation Analysis (GSVA) were performed to characterize biological themes. Immune infiltration was quantified with CIBERSORTx and single-sample Gene Set Enrichment Analysis (ssGSEA). Single-cell RNA-seq data (GSE216651) were employed for orthogonal validation. For experimental corroboration, synovial tissue was collected from OA patients undergoing arthroplasty; mRNA and protein levels of hub genes were determined by qRT-PCR, Western blot and immunofluorescence. The destabilisation of the medial meniscus (DMM) mouse model was used for in vivo verification. Twenty-one high-confidence ARDEGs were identified. Analysis of the PPI network yielded ten hub nodes, six of which (, , , , and ) retained non-zero coefficients in the least absolute shrinkage and selection operator (LASSO) model. Enrichment analyses implicated these genes in embryonic development, collagen-containing extracellular matrix remodeling and PI3K-Akt signaling. Immune infiltration analysis showed potential differences in immune cell abundance between OA and healthy controls. Single-cell dataset analysis verified the expression patterns of key genes in different cell types. Concordant dysregulation of , , , and was observed at both mRNA and protein levels in human OA synovium and DMM mouse joints. This comprehensive analysis identified acetylation-related genes and analyzed their potential biological roles in OA. The identified ARDEGs may provide new insights into OA diagnosis and treatment. - Source: PubMed
Publication date: 2026/08/11
Huang QiaojunZhao XiaoyiLong DianboLi MingJiang YiyiDiao HengyiChen WeishenMeng Fangang - Viral transcripts generate chimeric RNAs through fusion with host transcripts, modulating viral infection and host immune responses. Grass carp hemorrhagic disease, caused by grass carp reovirus (GCRV), represents a severe disorder threatening grass carp aquaculture. Previous research on GCRV-host interactions focused on viral and host protein crosstalk, with chimeric RNAs rarely reported. Here, 88 non-redundant GCRV-grass carp chimeric RNAs were identified using RNA-seq. Six chimeric RNA subtypes formed by the S5 segment RNA of GCRV and the early growth response 1 (EGR1) RNA of grass carp were detected by PCR and Sanger sequencing. Sequence analysis revealed short direct repeats at two parental RNA breakpoints, with merely one copy retained in the chimeric RNA. Among six subtypes, the upstream sequence of the S5 RNA breakpoint (243-324 nt) was connected with the downstream sequence of the egr1 breakpoint (2604-3111 nt) to form the chimeric RNA S5-AGUGA-EGR1. S5-AGUGA-EGR1 formation was independent of viral RNA-dependent RNA polymerase (RdRP) yet relied on the short direct repeat AGUGA at breakpoints. Functional assays revealed that S5 RNA formed S5-AGUGA-EGR1 by acquiring a partial sequence of the 3'-untranslated region (3'-UTR) of EGR1, leading to downregulated EGR1 expression and increased viral RNA levels. Furthermore, S5-AGUGA-EGR1 promoted viral genes expressions by encoding a GCRV-grass carp chimeric protein VP5-c (a truncated VP5 with 8 amino acid residues encoded by the 3'-UTR of egr1 at the C-terminal). These findings provide an unprecedented perspective on GCRV-grass carp interactions and identify a novel mechanism underlying viral RNA-mediated regulation of host gene expression. - Source: PubMed
Publication date: 2026/08/25
Shen ZeenQi YanlingZhang YiyangLi LiuyangLiu ZhuoZhang XingQian HeyingZhu MinHu XiaolongGong Chengliang - Interleukin-11 (IL-11), a member of the glycoprotein-130 cytokine family, has been implicated in inflammation-associated malignancies, including pancreatic cancer, where both IL-11 and its receptors are frequently overexpressed; however, the transcriptional mechanisms that regulate IL-11 expression remain unclear. To investigate this mechanism, promoter reporter assays, electrophoretic mobility shift assays, EGR1 knockdown experiments, gene expression analyses and three-dimensional spheroid invasion assays were performed in pancreatic cancer cells. In the present study, early growth response 1 (EGR1) was identified as a key regulator of insulin-like growth factor 1 (IGF-1)-induced transcription. Promoter analyses revealed a conserved EGR1-binding sequence (EBS) within the proximal promoter that is essential for IGF-1-responsive transcriptional activation. Electrophoretic mobility shift assays demonstrated that EGR1 directly binds to this site. Functional silencing of EGR1 markedly attenuated IGF-1-induced IL-11 expression and reduced invasive behavior in a three-dimensional pancreatic cancer spheroid model. Collectively, these findings delineated an IGF-1/EGR1/IL-11 signaling axis linking growth factor-dependent transcriptional regulation to invasive phenotypes and highlighted a potential therapeutic target in pancreatic cancer. - Source: PubMed
Publication date: 2026/08/13
Choi YenaJung EuitaekHan JunekyuShin Soon Young - Non-convulsive status epilepticus (NCSE) accounts for 20 to 40% of all observed cases of status epilepticus in the intensive care unit, but its early cellular and molecular consequences remain poorly understood. Here, we investigated early dentate gyrus alterations after pilocarpine-induced NCSE, focusing on whether neuroblast misplacement is associated with loss of Reelin-positive hilar interneurons or with functional impairment of Reelin signaling. Using cellular, molecular and imaging analyses, we found that NCSE was associated with reduced positioning of DCX-positive neuroblasts in the granule cell layer and diminished contacts between DCX-positive neuroblasts and GFAP-positive radial glia-like cells. These alterations occurred in the absence of a significant reduction in the number of Reelin-positive hilar interneurons, but were accompanied by reduced extracellular Reelin intensity, altered Reelin processing, and accumulation of intracellular Reelin clusters. Thus, in contrast to more severe convulsive status epilepticus models in which interneuron loss is prominent, our data support an early NCSE phenotype dominated by functional impairment of Reelin signaling. Two-day bumetanide treatment improved selected post-NCSE alterations, including extracellular Reelin processing, RGL-neuroblast contacts, intracellular Reelin clustering and EGR1 expression in Reelin-positive interneurons, and is therefore used here as a pharmacological probe of chloride-transport-associated mechanisms rather than as definitive evidence for direct central NKCC1 inhibition or therapeutic efficacy. These findings highlight NCSE as a distinct pathological entity and suggest that chloride-transport-sensitive changes in interneuron functional state may influence Reelin signaling and neuroblast positioning after seizures. - Source: PubMed
Publication date: 2026/08/24
Garcia Marta SaezKarakus CemTessier MarineMagoncia EllenFinizio LauraneDi Scala CoralieRivera Claudio