ATF3, 1-181aa, Human, E.coli
- Known as:
- ATF3, 1-181aa, Human, E.coli
- Catalog number:
- ATGP1127
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- ATF3 1-181aa Human .coli
Related genes to: ATF3, 1-181aa, Human, E.coli
- 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
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: ATF3, 1-181aa, Human, E.coli
Related articles to: ATF3, 1-181aa, Human, E.coli
- RNA modifications, especially N6-methyladenosine (m6A), have emerged as pivotal regulators of gene expression in neurological disorders, yet their roles in ischaemic stroke remain unclear. Here, we performed a CRISPR-Cas9 loss-of-function screen targeting 118 RNA modification-related genes in neuronal cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) and validated the findings in a mouse model of middle cerebral artery occlusion/reperfusion (MCAO/R). We identified Fto as a top negatively selected gene, with its expression progressively reduced and global m6A levels increased during ischaemic injury. Neuron-specific Fto knockout aggravated infarct size, neurological deficits, cognitive impairment, and neuronal apoptosis, accompanied by activation of multiple signalling pathways revealed by RNA-seq analysis. Integrated m6A-seq and RNA-seq profiling uncovered Atf3 as a hypermethylated and upregulated hub gene downstream of Fto deficiency, linking m6A dysregulation to enhanced neuronal apoptosis. In vitro assays confirmed that FTO knockdown increased ATF3 mRNA methylation and expression under OGD/R conditions, whereas Fto overexpression in vivo alleviated ischaemic brain injury, improved neurological outcomes, reduced Atf3 expression, and lowered global m6A levels. Together, our findings reveal the Fto/m6A/ATF3 axis as a critical mediator of ischaemic injury and highlight Fto restoration as a potential therapeutic strategy for stroke. - Source: PubMed
Publication date: 2026/10/05
Yu JiangtaoZhu XiaoluLu QianyuMa HaoliZhang ZhongxiangYu QianLiu ZilinLi ZhiqiangLi GangJin Xiaoqing - Benzene exposure is associated with increased cardiovascular disease (CVD) risk, yet the mechanisms linking benzene to vascular injury remain incompletely understood. Here, we investigated the effects of benzene and its reactive metabolite trans,trans-muconaldehyde (MA) on endothelial activation and leukocyte recruitment, early events in atherogenesis. Wild-type and endothelial-specific heat shock protein A1B overexpressing (EC-HSPA1B-TG) mice were exposed to inhaled benzene (1 ppm), and leukocyte dynamics were assessed by intravital microscopy. Complementary studies in vitro examined MA-induced endothelial activation via leukocyte adhesion assays, RNA sequencing, pharmacological interventions, and siRNA-mediated gene silencing. Benzene inhalation increased leukocyte rolling (16-21-fold) and adhesion (11-44-fold) in vivo with female mice exhibiting greater responses than males. In vitro, MA enhanced monocyte adhesion (1.7-fold) and transmigration (1.4-fold) and induced a conserved transcriptional program characterized by activation of oxidative stress, unfolded protein response (UPR), MAPK signaling, and heat shock pathways. MA stimulated phosphorylation of p38, JNK, and eIF2α, increased XBP1 splicing, elevated reactive oxygen species generation, and depleted glutathione. Alleviation of ER stress with 4-phenylbutyric acid attenuated MA-induced expression of HSPA1B, ATF3, and ICAM1. Conversely, HSPA1B silencing exacerbated endothelial activation and stress signaling, whereas endothelial-specific overexpression of HSPA1B significantly reduced benzene-induced leukocyte recruitment in vivo. Collectively, these findings identify proteotoxic stress as a central mechanism of benzene-induced vascular toxicity. Further, we demonstrate that activation of the heat shock pathway (HSF1-HSPA1B) serves as a protective response that limits endothelial inflammation. These results provide new mechanistic insight into how environmental benzene exposure may promote vascular injury and CVD in humans. - Source: PubMed
Publication date: 2026/09/29
McFall Samantha AMalovichko Marina VWickramasinghe Nalinie STaylor Breandon SMalik Mohammad TConklin Daniel JZelko Igor NSrivastava Sanjay - Activating transcription factor 3 (ATF3) is an immediate-early basic leucine zipper transcription factor induced by diverse forms of cellular stress. Although ATF3 is often described as a "double-edged sword," that formulation alone does not explain why the same stress-responsive factor can accompany successful adaptation, regeneration, inflammation resolution, cell death, fibrosis, or tumor progression. Here, we synthesize evidence across neuronal injury, innate immunity, cardiovascular and metabolic stress, cancer, and fibrotic disease and propose that ATF3 is better understood as a context-dependent stress rheostat. We organize ATF3 biology around two complementary principles: a temporal/intensity threshold model, in which the duration and magnitude of the stress response influence whether ATF3 is embedded in adaptive or unresolved pathological programs, and a partner/context-switch model, in which transcriptional output is redirected by cell identity, interacting transcription factors, chromatin state, and the surrounding signaling environment. This framework resolves several apparent contradictions in literature. Transient ATF3 induction can enhance neuronal growth competence, restrain Toll-like receptor (TLR) signaling, and support tissue adaptation, whereas sustained or disease-specific ATF3 programs can contribute to metabolic dysfunction, fibrotic remodeling, or tumor invasion. Importantly, ATF3 expression should not be equated with ATF3 causality: in several settings it marks a stressed cell state while cell fate is determined by additional signaling nodes. We therefore critically evaluate translation. ATF3 is well established as an experimental marker of neuronal and tissue stress, but its broad inducibility, intracellular localization, temporal variability, and cell-state dependence limit its current value as a stand-alone clinical biomarker. Similarly, global activation or inhibition is unlikely to be a generally safe therapeutic strategy. Future development should prioritize cell-resolved ATF3 activity signatures, temporal pharmacodynamic measurements, and context-selective interventions that target the specific ATF3-centered network operating in a defined disease state. - Source: PubMed
Publication date: 2026/09/25
Huang RongLi RuikangSaw Phei ErZhou Mao - Annulus fibrosus (AF) rupture is a key structural event in intervertebral disc degeneration, but effective repair is hindered by the acidic, hypoxic and oxidative microenvironment of the avascular disc. Single-cell transcriptomic reanalysis and clinical AF specimens identified ferroptosis-associated redox imbalance as a prominent feature of advanced degeneration. Here, we developed an acid-responsive nanobot-integrated core-shell microneedle system for staged annulus fibrosus repair. The shell layer released TA@MgO metal-phenolic nanobots that consumed pathological H, generated O, and provided NIR-amplified redox buffering, thereby normalizing the early degenerative microenvironment. The core layer enabled sustained quercetin release to reinforce anti-ferroptotic and matrix-preserving effects. Mechanistically, TMH/QG+NIR suppressed ferroptosis in AF cells by epigenetically silencing ATF3 through DNMT3A-dependent promoter methylation, thereby relieving ATF3-mediated repression of SLC7A11 and restoring GPX4-dependent antioxidant defense. In a puncture-induced degeneration model, this system alleviated ferroptotic injury, improved AF integrity, preserved disc height and enhanced biomechanical resilience. These findings identify the DNMT3A-ATF3-SLC7A11 axis as a therapeutically tractable ferroptosis-regulatory pathway and establish a staged microenvironment-reprogramming strategy for AF repair. - Source: PubMed
Publication date: 2026/09/27
Tan LuZheng YanLan YueCheng ZhuoWang SiyaLi ChangqingWang YanqiuLiu Minghan - Pain is a complex process involving dynamic transcriptional changes in cells of the PNS and CNS following injury or inflammation. Among stress-inducible transcription factors, ATF3 has emerged as one of the most robust molecular markers of neuronal injury, particularly in sensory neurons of the DRG. Although ATF3 is widely used as an indicator of axonal damage in experimental pain models, its functional contribution to the initiation, maintenance, and resolution of pain remains poorly understood. Recent transcriptomic and functional studies suggest that ATF3 not only reflects neuronal stress but also orchestrates gene expression programs involved in axonal regeneration, neuroimmune communication, ion channel remodeling, and nociceptor plasticity. Moreover, ATF3 expression has been identified in non-neuronal cell populations, including Schwann cells and satellite glial cells, indicating broader roles in peripheral nerve repair and neuroinflammation. Despite the growing body of experimental evidence, the literature remains fragmented, and no consensus has yet been reached as to whether ATF3 primarily promotes adaptive regeneration or directly contributes to maladaptive pain signaling. This review aims to provide a comprehensive and critical overview of the current understanding of ATF3 biology in pain, building on evidence from transcriptomic and molecular analyses, experimental models of neuropathic, inflammatory, and cancer-associated pain, and emerging mechanistic insights into its role in pain-related neuronal plasticity. This review examines the regulation of ATF3 expression, its downstream transcriptional targets, its interactions with inflammatory signaling pathways, and its potential value as a therapeutic target. By consolidating current evidence and highlighting existing knowledge gaps, this review seeks to clarify the multifaceted role of ATF3 in pain pathophysiology. - Source: PubMed
Publication date: 2026/08/29
García-Domínguez Mario