Ask about this productRelated genes to: EGR1 antibody
- 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 antibody
Related articles to: EGR1 antibody
- Accurate identification of transcription factor binding sites (TFBSs) at single-nucleotide resolution remains a central challenge in deciphering gene expression regulatory networks. To improve the performance of existing computational models for predicting TFBSs across different cell types, we presented a deep learning model integrating channel and spatial attention mechanisms. In this study, we trained and tested the model using a comprehensive dataset that included ChIP-seq data from 51 groups, involving 10 core transcription factors (e.g., CTCF, EGR1, FOXA1) across 13 human cell lines (e.g., A549, GM12878, H1-hESC), and DNase-seq data from 13 datasets. The results demonstrated that this model exhibited superior performance across 23 TF-cell type combinations, achieving a mean area under the receiver operating characteristic curve (AUROC) of 0.986, with 91% of samples yielding an AUROC above 0.970. Additionally, the mean area under the precision-recall curve (AUPRC) reached 0.169, over 1,000-fold higher than the random baseline 0.000156. When compared to state-of-the-art models in the field, such as FactorNet, Leopard, and DeepGRN, our model outperformed them in terms of AUROC on nine shared TF-cell type datasets. Visualization analyses further confirmed that our model enabled accurate identification of cell-type-specific TFBSs. This study provides an efficient computational framework for precise cross-cell-type TFBS prediction, thereby facilitating in-depth investigations into gene expression regulatory mechanisms and the molecular pathogenesis of related diseases. - Source: PubMed
Feng Ji-HuaChen Zhong-XingKang Qi-LinLi Long-FeiYang Jia-HuiZhang Yu-Ting - Diabetic peripheral neuropathy (DPN) is a common chronic complication of diabetes mellitus, and Schwann cell dysfunction contributes to its pathogenesis and progression. IGF2BP2 is a single-stranded RNA-binding protein that has recently been identified as an m6A reader; however, its role and regulatory effects in Schwann cells during DPN remain largely unknown. In this study, we demonstrated that high-glucose exposure significantly increased IGF2BP2 levels in RSC96 cells and in the sciatic nerves of both type 1 and type 2 diabetic mice, accompanied by reduced autophagy and neurotrophin expression. Consistently, IGF2BP2 expression was associated with metabolic and immune-related parameters in patients with type 2 diabetes. Functionally, IGF2BP2 overexpression inhibited, whereas its downregulation partially rescued, high glucose-induced suppression of autophagy and neurotrophin expression in vitro (RSC96 cells) and in vivo (IGF2BP2 knockout mice). Mechanistically, IGF2BP2 bound to EGR1 mRNA in an m6A modification-dependent manner, primarily recognizing an adenosine at position 1268, thereby enhancing EGR1 mRNA stability. Downregulation of EGR1 alleviated the inhibitory effects of IGF2BP2 overexpression on autophagy and neurotrophin expression in RSC96 cells. Conversely, EGR1 overexpression attenuated the protective effects of IGF2BP2 knockout on peripheral nerve function and neurotrophic signaling in diabetic mice. Overall, high-glucose stimulation upregulated IGF2BP2, which enhanced EGR1 mRNA stability in an m6A-dependent manner, thereby suppressing autophagy and neurotrophin expression in Schwann cells during DPN. - Source: PubMed
Wei WandiLi FanJin TingtingLi QiuliGao YueYuwen ChaoSun YuanyuanLi WenhuiZhu LinHao Jun - There is a common basis of the diabetic nephropathy (DN) and diabetic retinopathy (DR), but the common genes of DN and DR were unclear. - Source: PubMed
Publication date: 2026/04/28
He JuanZhang DandanWang Yan - Studies examining the paracrine effect of fibroblasts on the myogenesis of bovine muscle satellite cells (MuSCs) have confirmed their stimulating effect on proliferation and early differentiation. However, traditional two-dimensional (2D) cell culture models fail to accurately represent the complexity of in vivo muscle tissue. This study aims to investigate the paracrine effect of fibroblasts on myogenesis in a three-dimensional (3D) cell culture model. Cells were cultured in monoculture and co-culture with fibroblasts in a spinner flask using gelatin microcarriers, Cultishper, which maximizes the growth surface area for adherent cells. Then, muscle cells from the co-culture were sorted by the FACS method based on negative expression of CD90, a fibroblast-associated marker. The progress of myogenesis was assessed based on qPCR analysis for selected muscle markers and at the protein level for skeletal myosin. Fluorescent staining and luminescent metabolic assays were performed to control culture conditions. The obtained results revealed up-regulation of genes involved in cell activation and proliferation (PAX7, MYF5, and MYOD) and differentiation (MYOG, EGR1, and MYH). Metabolism analyses did not show changes between mono- and co-culture conditions. To summarize, fibroblasts through paracrine signaling promote early differentiation of MuSCs and potentially proliferation, which provides valuable insights for the advancement of cultured meat production. - Source: PubMed
Publication date: 2026/05/11
Zygmunt KarolinaPiórkowska KatarzynaAdamiak JuliaWitarski Wojciech - Breast cancer therapy is compromised by widespread tamoxifen resistance. The modulatory role of Caspase14 in the early growth response protein 1 (EGR1)/hypoxia-inducible factor 1-alpha (HIF-1α) axis in this context is unclear. We investigated how Caspase14 regulates EGR1/HIF-1α to promote 4-hydroxytamoxifen (4-OHT) resistance in MCF7 cells using cell-based genetic and biochemical assays (small-interference RNA knockdown, plasmid overexpression, Western blotting, qPCR, IC50 assays, and Chromatin immunoprecipitation experiments) across multiple independent experiments. Caspase14 expression correlated with resistance, with IC rising from 0.178 µM to 1.575 µM in resistant variants. EGR1 knockdown reduced Caspase14 and downstream targets GLUT3 and BCRP, implicating EGR1 as a key mediator. Resistant cells displayed elevated HIF-1α that enhanced metabolism and migration, further supporting a role in drug resistance. These data indicate that Caspase14 promotes survival, proliferation, and metabolic reprogramming in resistant MCF7 cells via the EGR1/HIF-1α pathway. Our findings reveal a mechanistic link between Caspase14 and endocrine therapy resistance and nominate Caspase14 as a therapeutic target to overcome tamoxifen resistance, with potential translational relevance. - Source: PubMed
Publication date: 2026/05/11
Ji FeihuZhao AnpingChen QiuxuLi ChenweiHuang Liyuan