ATF3 antibody
- Known as:
- ATF3 (anti-)
- Catalog number:
- orb10154
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ATF3 antibody
Related genes to: ATF3 antibody
- 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 antibody
Related articles to: ATF3 antibody
- The age-related decline in liver regenerative capacity worsens outcomes for elderly patients with liver disease or undergoing liver surgery, and therapeutic options are limited. The RNA modification N4-acetylcytidine (ac4C), catalyzed by N-acetyltransferase 10 (Nat10), is implicated in regeneration; however, its role in the aged liver remains unknown. - Source: PubMed
Publication date: 2026/06/18
You QiangXiao CuicuiChen HaoqiZhang GongmingZhang FengWu ZhengqiLiu YasongZhang JiebinChen HaitianXiao JiaqiChen WenjieYao JiaZhang YingcaiLi HuaLi HuiYang YangLi RongZheng Jun - Efficient brain-targeted gene delivery remains a formidable primary bottleneck in the clinical management of intracerebral hemorrhage (ICH). Herein, we engineered a dual-functional biomimetic nanoplatform (L57-NExos@saRNA) that synergizes active blood-brain barrier (BBB) penetration with intrinsic neuroregeneration. Guided by transcriptomic profiling, a small activating RNA (saRNA) was designed to upregulate activating transcription factor 3 (ATF3) -a critical repressor of the Toll-like receptor 4 (TLR4) neuroinflammatory cascade. To overcome formidable physiological barriers, the saRNA was condensed within neural stem cell-derived exosomes (NExos) surface-functionalized with the low-density lipoprotein receptor-related protein-1 (LRP1)-targeting peptide L57. By proactively exploiting the pathological upregulation of LRP1 on BBB-associated astrocytes following ICH, this L57-modified nanoplatform achieves highly efficient receptor-mediated transcytosis, ensuring robust and specific accumulation at the hemorrhagic lesion. Once internalized, the nanomedicine orchestrates a profound dual-therapeutic response. First, the delivered saRNA specifically reprograms microglia from a neurotoxic (M1) to a neuroprotective (M2) phenotype. This shift fundamentally rectifies maladaptive microglial-astrocyte crosstalk, subsequently driving reactive astrocytes toward an A2 protective state to deeply detoxify the inflammatory microenvironment. Concurrently, the bioactive NExos carrier itself transcends its role as a mere vehicle by activating the PI3K/Akt survival pathway, directly inhibiting neuronal apoptosis and facilitating network repair. By seamlessly converging precise BBB-targeted gene regulation with biomimetic carrier-driven repair, this versatile delivery system presents a highly translational and promising therapeutic paradigm for ICH. - Source: PubMed
Publication date: 2026/06/18
Xu LixingSong YanTao HuiminNi LuyunHuang HaiqinShen Jiabing - New half-sandwich iridium(III) compounds [Ir(η-Cp)Cl(L1-3)]PF (-), combining Cp* or Cp with N,P-coordinated phosphinoalkylamines L1-L3, were tested in different cancer cells (2D and 3D cultures), including MOR/CPR cisplatin-resistant lung carcinoma. Best-performing compound outperformed its Cp analogue and cisplatin in MOR/CPR cells while sparing noncancerous cells. Multiomics profiling shows a non-DNA-targeted mechanism: rapid integrated stress response with ER stress (DDIT3/CHOP) and oxidative stress (HMOX1, ATF3), nucleolar stress, and primary inhibition of ribosome biogenesis and mitochondrial translation. These changes drive translational shutdown, suppression of oxidative phosphorylation with a glycolytic shift, and G arrest, alongside endolysosomal remodeling (enhanced vesicular uptake, reduced degradative capacity) that favors intracellular retention. The phenotype is predominantly cytostatic with apoptotic priming. In vivo, suppressed tumor growth and activated apoptosis with low systemic toxicity. Compound thus emerges as a promising prototype Ir(III) metallodrug that disrupts nucleolar, mitochondrial, and lysosomal homeostasis to overcome resistance. - Source: PubMed
Publication date: 2026/06/16
Štarha PavelFriedecká JaroslavaHéžová RenataBárta OndřejJarošová ReaMašek JosefNemec IvanMilde DavidNovobilský AdamNovotný LadislavOndruš JaroslavŠterbinská SlavomíraStraková NicolLenobel RenéHošek Jan - Atopic dermatitis (AD) is a common and chronic inflammatory skin disease with global prevalence. Its clinical heterogeneity and complex molecular mechanisms pose significant challenges for the development of effective therapies. To explore AD molecular heterogeneity using lesional skin transcriptomic data, characterize their biological and immune profiles, and identify key genes underlying the differentiation. Differentially expressed genes were identified using DESeq2, followed by pathway and co-expression analyses via GSEA and WGCNA, respectively. Mitochondrial-related genes were extracted by intersecting DEGs and WGCNA modules with the MitoCarta3.0 database, and their functional relevance was assessed through GO and KEGG enrichment. Hub genes were identified by protein-protein interaction network analysis, which were subsequently used to construct a classification model. Transcriptional regulators were predicted using hTFtarget, while immune cell infiltration was quantified using CIBERSORT. Two molecular subgroups were identified. Cluster 1 was enriched in cell signaling and adhesion pathways, whereas Cluster 2 exhibited upregulation of oxidative phosphorylation and proteasome-related processes. A total of 85 mitochondrial-associated genes, primarily involved in energy metabolism, were differentially expressed between clusters. PPI network analysis identified four hub genes (BAD, BOLA1, CHCHD5, and ISOC2), which were significantly upregulated in Cluster 1. A hub gene-based classifier demonstrated strong discriminatory power (area under the curve > 0.7). Predicted key transcriptional regulators included ATF3, BRD2, BRD4, and CEBPA. Immune profiling revealed higher regulatory T cell infiltration in Cluster 1 and increased follicular helper T cells in Cluster 2. This study reveals two molecularly and immunologically distinct AD subtypes, characterized by differential mitochondrial function and immune microenvironment signatures. - Source: PubMed
Publication date: 2026/05/26
Yu YingyaoShang YuanyuanGe XinhongDong LingdiLi Kexin - Urolithin C (UC), a natural compound derived from the metabolism of ellagitannins by gut microbiota, exhibits diverse pharmacological and biological activities. However, its therapeutic potential and underlying mechanisms in endometrial cancer (EC) remain unclear. Functional assays were used to determine the effects of UC on the viability, proliferation, cell cycle, apoptosis, migration, and autophagy in EC cells. RNA sequencing was used to investigate the effect of UC on total gene expression in EC cells. The expression level of activating transcription factor 3 (ATF3) was evaluated using western blotting, real-time PCR, and immunofluorescence staining. Organoids and a mouse model of EC were used to analyze the anti-tumor effects of UC. UC significantly inhibited the malignant behavior of EC cells. High-throughput transcriptome sequencing revealed a close association between autophagy and UC treatment, and identified ATF3 as a key downstream factor. UC treatment increased the expression of ATF3, which was primarily localized to the nucleus. Elevated ATF3 levels positively correlated with the survival of patients with EC. ATF3 knockdown rescued the effects of UC on cell viability, migration, and autophagy. Furthermore, EC organoid and in vivo experiments showed that UC markedly reduced organoid viability and EC tumor growth. UC exerts anti-EC activity by promoting ATF3 expression, thereby inhibiting the malignant behavior of EC cells and promoting autophagic cell death. - Source: PubMed
Hu RuiqiLiu CuilanDong XiangyuDu HengweiBi RuixueZhang YantingWang XinjingLiu XueyuanChen WeiweiWang FeiCui BingjieDong HongliangWang YiDu JingLiu Zhiqiang