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
- Acute pancreatitis (AP) is an inflammatory disorder with no efficient therapy. Here we demonstrate that the anorexigenic peptide nesfatin-1 exerts potent and dose-dependent protection against both caerulein-induced and hypertriglyceridemic AP. Intraperitoneal administration of nesfatin-1 to restore its serum levels significantly reduced pancreatic necrosis, edema, and infiltration of immune cells, as well as circulating levels of amylase, lipase, and pro-inflammatory cytokines. RNA-seq revealed that nesfatin-1 down-regulated the ER-stress signature (Ddit3, Atf3, Ppp1r15a) and the NF-κB/NLRP3 signaling. Further studies in primary acinar cells confirmed that nesfatin-1 at the dose of 10 nM suppressed phosphorylated eIF2α, DDIT3, ATF3, p65, and NLRP3, thereby inhibiting pyroptosis. Consequently, nesfatin-1 attenuated macrophage/neutrophil infiltration, shifted M1 toward M2 macrophages, inhibited the release of inflammatory cytokines, and alleviated multi-organ injury in lung, intestine, and spleen. Collectively, nesfatin-1 limits AP severity by restraining ER-stress-driven pyroptosis and innate immune activation. Thus, nesfatin-1 may serve as a promising therapeutic candidate for acute pancreatitis. - Source: PubMed
Li HanWang XianfengNiu YuefengSun LijunYang YinmoZhang WeizhenYin Yue - Activating transcription factor 3 (ATF3) is a stress-inducible transcription factor that regulates inflammatory responses; however, its cell-type-specific role in liver fibrosis remains incompletely defined. We investigated the function of myeloid cell-specific ATF3 in carbon tetrachloride (CCl)-induced liver fibrosis. ATF3 induction was confirmed in bone marrow-derived macrophages following lipopolysaccharide stimulation in vitro. Myeloid-specific Atf3 knockout mice (Atf3 LysM-Cre+) and littermate controls were subjected to CCl treatment to determine the impact of ATF3 loss in vivo. Myeloid ATF3 deficiency significantly exacerbated CCl-induced liver injury, reflected by elevated serum ALT and AST levels, increased collagen deposition, and higher fibrosis scores. ATF3 loss enhanced hepatic stellate cell activation, as evidenced by increased α-SMA protein and elevated Acta2 and Col1a1 expression. Although total macrophage abundance was unchanged, ATF3 deficiency shifted macrophage composition toward increased Ly6C+ infiltrating monocyte-derived macrophages and reduced Kupffer cell markers. Mechanistically, Atf3-deficient livers displayed increased inflammatory chemokine expression (Ccl3, Ccl4, Ccl5, Ccl8), reduced matrix metalloproteinases (Mmp2, Mmp8, and Mmp9), increased tissue inhibitor of metalloproteinases 1 (Timp1), and enhanced activation of transforming growth factor-beta1 (TGF-β1)/SMAD signaling. These findings identify myeloid ATF3 as a protective regulator that restrains inflammatory amplification and extracellular matrix accumulation during liver fibrosis. Modulation of ATF3-dependent pathways may represent a potential therapeutic strategy for fibrotic liver disease. - Source: PubMed
Ling HaoHu YanzhuOnyuru JansetShi JingSteffani MarcellaWang JianyeWasmaier LenaSchulze SarahMäritz NadjaXin ZhengyiFriess HelmutHolzmann BernhardHüser NorbertStoess ChristianHartmann Daniel - Silicosis is the most common occupational lung disease caused by respirable crystalline silica inhalation, with limited therapeutic options. Cellular senescence plays a critical role in the pathogenesis of lung diseases, while the role of senescent macrophages in silicosis remains unclear. Single-cell RNA sequencing (scRNA-seq) of healthy and silicosis human and mouse lung tissues revealed that activating transcription factor 3 (ATF3)-mediated macrophage senescence is closely linked to silicosis progression. Mechanistically, Sirtuin 6 (SIRT6)-mediated ATF3 deacetylation enhanced its nuclear transport and subsequently activated mitochondria-localized glutamic acid-rich protein (MGARP) transcription, thereby causing mitochondrial dysfunction and macrophage senescence. Senescent macrophages promoted fibroblast activation via the secreted phosphoprotein 1 (SPP1)-cluster of differentiation 44 (CD44) signaling pathway. Furthermore, the nuclear transport protein importin α and the molecular chaperone protein heat shock protein 70 (HSP70) competitively bound to ATF3, preventing its lysosomal degradation while promoting its nuclear import during macrophage senescence. Moreover, the small-molecule inhibitor Itraconazole, which targets the binding site of ATF3 and importin α, could reduce ATF3 nuclear entry, macrophage senescence, and pulmonary fibrosis (PF). Collectively, our study provided insights into the mechanism by which deacetylated ATF3 facilitates silicosis progression via increased nuclear transport and macrophage senescence, and indicated potential therapeutic targets for PF. - Source: PubMed
Publication date: 2026/05/20
Cheng DeminBu WenxiaWang FengxuJin YueyuanLiu RongzhuZhao RuiWang XuehaiJiang MengnaShen JinpingCheng XinhangChen ZumingZhu LiLi JinlongGe ZhenzhongMiao ShichenXu HaotianZhou XiaoyuWang DongmingZhao Xinyuan - Autism spectrum disorder (ASD) is a neurodevelopmental disorder marked by repetitive behaviors and difficulties in social interaction and communication. The pathogenesis of ASD remains poorly understood, and no definitive treatment is currently available. This study aimed to systematically identify key genes and signaling pathways involved in autistic-like behaviors by performing genome-wide transcriptional profiling on a neonatal maternal separation (NMS) rat model, thereby revealing the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/28
Zhang QingMa JinhuaXu BoqingLi XiaohuanDai ChunfangZhu LiqiongDing Xiaoting - Class IIa histone deacetylase 7 (HDAC7) regulates transcription primarily through scaffolding functions, but its molecular mechanisms in cancer pathogenesis remain incompletely understood. Here, we establish HDAC7 as a key epigenetic regulator in colorectal cancer (CRC). HDAC7 is overexpressed in CRC tumors and correlates with advanced disease stages, lymph node metastasis, and poor patient survival. Mechanistically, HDAC7 scaffolds a repressive complex with HDAC3 and the stress-responsive transcription factor ATF3. This reduces H3K27ac/H3K18ac occupancy and blocks BRD4/RNA polymerase II (Pol II) recruitment at regulatory regions to epigenetically silence its transcription. Consequently, this repression inactivates ATF3's tumor-suppressive functions, activating oncogenic PI3K-Akt signaling while suppressing the Hippo pathway. Genetic depletion or pharmacological inhibition of HDAC7 disrupts this repressive complex, triggering a functional switch in ATF3. This promotes BRD4/Pol II recruitment and H3K27ac enrichment at the ATF3 locus, enabling ATF3 to undergo transcriptional self-activation. Reactivated ATF3 suppresses CRC proliferation and survival by downregulating Bcl-2, upregulating p21 () to induce cell cycle arrest, promoting caspase-3-mediated apoptosis, and inhibiting PI3K-Akt signaling. Xenograft studies confirm that HDAC7 depletion suppresses tumorigenicity . Our work identifies HDAC7 as a molecular mediator that governs ATF3's functional plasticity through competitive cofactor recruitment, positioning HDAC7 inhibition as a therapeutic strategy to reactivate ATF3-mediated tumor suppression in CRC. - Source: PubMed
Publication date: 2026/05/01
Wang QiJi DongleiJia YanjieLi ShuangGao WenjingLiang TingtingLiang YingyingZeng CarolineWang ChunyuCheung Ka LungWang QuanZhou Ming-MingZeng Lei