ATF3
- Known as:
- ATF3
- Catalog number:
- 000186A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATF3
Related genes to: ATF3
- Gene:
- ATF3 NIH gene
- Name:
- activating transcription factor 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-03
- Date modifiied:
- 2014-11-19
Related products to: ATF3
Related articles to: ATF3
- Repeated implantation failure (RIF) remains a significant challenge in assisted reproductive technology. Endometrial receptivity (ER) plays a critical role in embryo implantation. However, the impact of advanced maternal age (AMA) on ER in this population remains unclear. The study aimed to evaluate whether maternal age is associated with displacement of the window of implantation (WOI) and explore potential endometrial transcriptomic characteristics. - Source: PubMed
Publication date: 2026/08/26
Guo YapingZhang MianqiuWu ZhenggangHou XiaojingZhang JuanYang XiaoxuanDing HuiJi ChenboLing XiufengSu YanShen Rong - Osteosarcoma (OS) is highly invasive, metastatic, and lacks effective therapies, leading to poor prognosis. This study aims to dissect the core epigenetic features of OS from the perspective of chromatin accessibility to elucidate its pathogenesis and identify novel therapeutic targets. ATAC-seq was used to map the global chromatin accessibility profiles of OS tissues versus normal controls. We identified OS-specific aberrantly accessible chromatin regions and delineated enriched transcription factor binding motifs. Key transcription factors were validated by Western blotting and flow cytometry. Notably, in regions with enhanced accessibility, the binding probability of AP-1 family members (including Atf3, Fra1, Fra2, JunB, BATF, AP-1, Jun-AP1, Bach2, and CTCF) was significantly elevated. Further analysis indicates that JunB can inhibit apoptosis of OS cells and enhance their invasive ability, suggesting that it may be related to tumor progression. Overall, JunB, as a candidate molecule with potential research value, is worthy of further verification in subsequent in vivo models and clinical samples to determine its feasibility as an intervention target for OS. - Source: PubMed
Publication date: 2026/09/05
Ye FanHu Po - To determine whether polymorphisms can serve as genetic biomarkers for machine learning-based precision analgesia by establishing a genotype-phenotype association suitable for predictive modeling of postoperative opioid requirements. - Source: PubMed
Publication date: 2026/09/02
Zhou ShilianLin ZhongyuanWang XiangZhang XinyuZhou YilingWang DiyaShu HaihuaYe Fang - Nutrient deprivation in the tumor microenvironment drives metastatic progression. However, its role in breast cancer metastasis and underlying epigenetic mechanisms remain unclear. We identify an enhancer-driven transcriptional program that promotes breast cancer metastasis under nutrient deprivation. Transient glucose-glutamine deprivation in MCF7 and MDA-MB-231 cells induces the expression of genes involved in migration, invasion, and metastasis. Chromatin immunoprecipitation sequencing shows distinct enhancer activation, marked by increased histone H3 lysine 27 and bromodomain-containing protein 4 (BRD4) recruitment. Targeted enhancer acetylation using dCas9-p300 increases cognate gene expression. Motif and CUT&RUN analyses indicate the enrichment and direct binding of ATF3 and c-JUN at enhancers-essential for their activation. Transient transcriptome sequencing shows an increase in endothelin 1 (EDN1) enhancer RNA (eRNA) transcription to facilitate enhancer activation, which is reduced by treatment with eRNA-targeting antisense oligonucleotides (ASOs). In an orthotopic mouse model, BRD4 inhibition using JQ1 or MZ1 suppresses 4T1 cell metastasis. EDN1 enhancer acetylation with dCas9-p300 increases MCF7 tumor growth, which is reduced by BRD4 inhibition or ASO treatment. BRD4 and EDN1 expression is commonly upregulated in human breast metastasis. These findings define nutrient stress-responsive enhancers as epigenetic drivers of metastatic adaptation and highlight their therapeutic potential in breast cancer. - Source: PubMed
Publication date: 2026/08/29
Bhattarai Poshan YugalVasukutty ArathyNa YujinLim Sung-ChulChoi Hong Seok - 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