Ask about this productRelated genes to: STAT3 antibody
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT3 antibody
Related articles to: STAT3 antibody
- An elevated risk for inflammatory bowel disease (IBD) has been linked to the intake of high-fat diet (HFD), yet the underlying molecular mechanisms remain unclear. The lysosome and the macroautophagy/autophagy-lysosome pathway (ALP) are critical for maintaining the intestinal epithelial barrier. By employing both an in vivo model of dextran sulfate sodium (DSS)-induced colitis in mice and an in vitro model using lipopolysaccharide (LPS)-treated NCM460 cells, we established that HFD in vivo and palmitic acid (PA) in vitro profoundly impair epithelial barrier function and amplify inflammation, which was linked to the suppression of lysosomal function and the ALP. Mechanistically, HFD in vivo and PA in vitro activated STAT3 (p-STAT3[Y705]) under DSS- and LPS-associated inflammatory stress, respectively. This led to a dual suppression of TFEB: on the one hand, activated STAT3 directly bound to the promoter to inhibit its transcription; on the other hand, it facilitated the lysosomal recruitment of MTOR and activated MTORC1, which promoted TFEB phosphorylation (p-TFEB[S211]) and hindered its nuclear translocation. This cascade resulted in lysosomal membrane permeabilization (LMP), loss of acidification, and impaired degradative function. Intestinal epithelial-specific knockout of or pharmacological activation of TFEB restored lysosomal function, repaired the epithelial barrier, and ameliorated colitis. Conversely, rectal administration of AAV9- reversed the protective effects conferred by knockout. Our study reveals that HFD in vivo and PA in vitro disrupt lysosomal function and the intestinal barrier through the STAT3-TFEB axis, suggesting this signaling pathway as a promising avenue for intervention in diet-associated IBD. Abbreviations: AB-PAS: Alcian blue-periodic acid-Schiff; ALP: autophagy-lysosome pathway; CD: Crohn disease; ChIP: chromatin immunoprecipitation; CLEAR: coordinated lysosomal expression and regulation; DSS: dextran sulfate sodium; HFD: high-fat diet; IBD: inflammatory bowel disease; IF: immunofluorescence; IHC: immunohistochemistry; LAMP: lysosome associated membrane protein; LGALS3/Gal3: galectin 3; LMP: lysosomal membrane permeabilization; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin kinase complex 1; PA: palmitic acid; RRAG: Ras-related GTP binding; RRAG-CA: constitutively active RRAG GTPase; RT-qPCR: reverse transcription quantitative PCR; SQSTM1/p62: sequestosome 1; STAT3: signal transducer and activator of transcription 3; TA1: TFEB activator 1; TEM: transmission electron microscopy; TFEB: transcription factor EB; TJ: tight junction; TUNEL: terminal deoxynucleotidyl transferase dUTP nick-end labeling; UC: ulcerative colitis; WB: western blot; WT: wild-type. - Source: PubMed
Publication date: 2026/05/21
He HaodongGuo XingZhouXu MiaoTan ZongbiaoTan ChenLi XiangyunXiang ZixuanHe PengzhanDeng BeiyingPu YuLiu YafeiZhang LuyunZhang JixiangDong Weiguo - Microcystin-LR (MC-LR), an emerging contaminant present in aquatic environments, poses health risks owing to its widespread distribution, bioaccumulation potential, and well-documented human exposure. However, its impact on endometrial function during early pregnancy remains poorly understood. This study investigates the effects and mechanisms of MC-LR exposure during the peri-implantation period on endometrial receptivity. Pregnant mice were administered with MC-LR at a biologically relevant dose (1/2 NOAEL, 20 μg/kg/day) from gestational days 3.5 to 5.5. MC-LR exposure impaired uterine morphology, reduced serum progesterone, and suppressed expression of key receptivity markers, resulting in decreased implantation sites. Transcriptomic analysis revealed dysregulation of the extracellular region, immune response, and hormone activity, with STAT3 signaling identified as a key regulator. MC-LR also disrupted uterine immune homeostasis, causing macrophage dysfunction and reduced IL-6 levels. The IL-6-dependent STAT3/HIF-1α signaling pathway was inhibited by MC-LR but reactivated by Garcinone D. Pharmacological activation of STAT3 prevented MC-LR-induced impairments, including cytokine dysregulation, extracellular matrix degradation, angiogenesis inhibition, reduced gland numbers, and decreased implantation capacity, though serum progesterone levels remained unaffected. These findings suggest that MC-LR disrupts endometrial receptivity via STAT3/HIF-1α signaling, independent of progesterone restoration, providing novel insights into microcystin-induced reproductive toxicity and a potential therapeutic target for implantation failure. - Source: PubMed
Publication date: 2025/12/21
Guo YaoLiu HaohaoZhang ZongxinChen XinghaiWang WenjunDu Xingde - Atherosclerosis (AS) progression is closely associated with phenotypic transformation of vascular smooth muscle cells (VSMCs) and activation of the Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) signaling pathway. This study aimed to elucidate the active components and underlying mechanisms of the Tiaozhi Tongmai Formula (TZTMF) in ameliorating AS through both in vivo and in vitro experiments. - Source: PubMed
Publication date: 2026/03/27
Zhang LuMaimaiti KaidinuerSun Jia-LiZhang Meng-MengZhang Min-Yu - STAT3 signaling is fundamental to T cells, where it underlies basic cellular processes like metabolism and apoptosis, as well as specialized processes like effector differentiation and cytokine production. However, mutations of STAT3 are strikingly prevalent in T-cell cancers, and aberrant or excessive STAT3 signaling is thought to mobilize cellular pathways that encourage malignancy. To better understand how STAT3 mutations drive T-cell cancers, we compared two frequent cancer-associated variants, Y640F and N647I, at the cellular and molecular levels. Using a retrogenic system, we demonstrate that they are qualitatively similar yet quantitatively distinct; each bears a gain-of-function phenotype, but Y640F has greater transcriptome-wide effects. We also discovered that these and other common STAT3 mutants invoke a T regulatory 1 (Tr1) gene program characterized by expression of IL-10 and other factors that dampen T-cell responses, including LAG3 and CD39. Importantly, "Tr1 skewing" is evident in both mouse T cells expressing cancer-associated STAT3 variants and humans afflicted with T-cell malignancies. These studies advance current understanding of how cancer-associated mutations impact STAT3 function and reveal anti-inflammatory properties that may help transformed T cells persist, expand, and/or avoid eradication. - Source: PubMed
Publication date: 2026/05/05
Schultz Aaron BDalzell MollyNivelo LuisHenrickson Sarah EVillarino Alejandro V - 23-Hydroxybetulinic acid (23-HBA), a key bioactive compound in the traditional Chinese herb , has garnered substantial scientific interest due to its potent antitumor activity. However, the inhibitory effects of 23-HBA on esophageal cancer growth have not been fully elucidated. - Source: PubMed
Publication date: 2026/05/05
Yang HuiSi GaoZhou XiSong XuejieDu HaiyangSi Fuchun