ATF3 CMV Expression Vector
- Known as:
- ATF3 cytomegalovirus Expression Vector
- Catalog number:
- ME0055
- Product Quantity:
- 15 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ATF3 CMV Expression Vector
Related genes to: ATF3 CMV Expression Vector
- 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 CMV Expression Vector
Related articles to: ATF3 CMV Expression Vector
- 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 - Ischemic brain injury is a major contributor to global mortality and disability. Despite extensive pathological characterization, systematic integration of rodent transcriptomic data remains limited. This study investigates orthologous transcription factors (TFs) in cerebral ischemia models and their roles in regulating neuroinflammation to develop novel diagnostic and/or predictive biomarkers. - Source: PubMed
Publication date: 2026/08/11
Xu HuiHuang XuHong Ming-YangXu JianYang Tao-TaoShi Rui-RuiGu Jin-Hua - [This corrects the article DOI: 10.3389/fnmol.2025.1554802.]. - Source: PubMed
Publication date: 2026/08/07
Li HaifengqingZhang FanZhang CongZhou MinLiu QingZeng Guoyong - 6PPD-quinone (6PPDQ), a tire-derived environmental toxicant, is closely associated with liver injury, but its toxicological mechanisms remain unclear. Selenium (Se), an essential trace element with antioxidant and cytoprotective properties, has shown potential in mitigating chemically induced liver injury. In this investigation, the protective effects of Se supplementation in 6PPDQ-induced hepatotoxicity were examined and the underlying mechanisms were elucidated by constructing both mice and AML12 cell models. The results demonstrated that 6PPDQ promotes liver inflammation by activating necroptosis. ATF3, a stress-inducible transcription factor, served as a key mediator of 6PPDQ-induced liver necroptosis. ATF3 nuclear translocation was driven by ROS and its expression regulated by METTL3/YTHDC1-mediated m6A methylation. Notably, selenomethionine (SeMet) effectively alleviated 6PPDQ-induced liver necroptosis by reducing ROS production, thereby suppressing ATF3 nuclear translocation and inhibiting the METTL3/YTHDC1-mediated m6A modification. These findings provide novel mechanistic insights into 6PPDQ hepatotoxicity and highlight the protective role of selenium against environmentally induced liver damage. - Source: PubMed
Li BoFu Hong-YuYin YishanJiang XuehanXiao BangWang SiwenZhang DuoChen XiaoxiaoJing YimingShi BendongZhang Ziwei - MYCN is a key oncogenic driver in hepatocellular carcinoma (HCC) and a therapeutic challenge due to the historical undruggability of MYC transcription factors (TFs). Using a high-throughput promoter-luciferase reporter, we identified PhiKan 083 (PK83), a small molecule previously recognized as a mutant p53 activator, that dose-dependently suppresses expression in HCC cells. PK83 impaired the proliferation and survival of MYCN-high HCC cells, inducing DNA damage, apoptosis, and loss of clonogenic and spheroid growth potential, while sparing MYCN-low HCC cells and normal hepatocytes. Structure-activity analysis revealed that polar, hydrogen-bond-capable substituents on PK83's tricyclic scaffold are critical for its activity. Although PK83 broadly activates p53 signaling, its cytotoxicity in MYCN-high cells is not strictly dependent on intact p53, as confirmed in p53-knockout systems. Transcriptome profiling and pathway analysis demonstrated robust suppression of MYC/MYCN targets along with modulation of pathways linked to stress, differentiation, and metabolism. In primary HCC tumors, PK83-downregulated TFs, including oncogenic TFs and , positively correlated with , whereas upregulated stress-responsive TFs and showed a negative correlation. These findings suggest that PK83 suppresses MYCN expression and preferentially affects MYCN-high HCC cells in a p53-independent manner, warranting further preclinical investigation of PK83 and related compounds in MYCN-associated cancers. - Source: PubMed
Publication date: 2026/07/18
Xu YaliMishra HrichaTakahashi MasatakaNishimura HajimeSuenaga YusukeYu WenkuiHippo YoshitakaSuzuki HarukazuQin Xian-Yang