STAT3 (Phospho_Ser727) Antibody
- Known as:
- STAT3 (Phospho_Ser727) Antibody
- Catalog number:
- E011046-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT3 (Phospho_Ser727) Antibody
Related genes to: STAT3 (Phospho_Ser727) 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 (Phospho_Ser727) Antibody
Related articles to: STAT3 (Phospho_Ser727) Antibody
- Despite newly introduced treatment options, the 5-year survival rate for non-small cell lung cancer (NSCLC) remains below 20%, indicating a remaining need for new treatment strategies. Benzamil (BZ) has demonstrated inhibitory effects on brain tumors and osteosarcoma; however, its effects on NSCLC cells remain unknown. In this study, we investigated the potential anti-cancer effects of BZ in a panel of NSCLC cell lines. Compared to cells with EGFR L858R/T790M double mutations (H1975), BZ induced greater cytotoxicity in EGFR wild-type (A549, H1299, H292) and EGFR ex19del (PC9) cells. Mechanistically, BZ treatment was associated with inhibition of Akt, ERK1/2, and Stat3 signaling and increased mitochondrial damage. It was also associated with reduced Drp1 and Fis1 expression. Moreover, BZ induced release of cytochrome c, Smac/Diablo, and HtrA2/Omi from mitochondria. Additionally, BZ enhanced osimertinib-induced cytotoxicity in EGFR-mutant cells, and it suppressed H1975-derived cancer spheres. These findings support a proposed model in which BZ-induced mitochondrial damage is accompanied by the release of cytochrome c, Smac/Diablo, and HtrA2/Omi. These changes were accompanied by caspase activation and cell line-dependent alterations in XIAP expression, consistent with their potential contribution to apoptosis in NSCLC cells. - Source: PubMed
Publication date: 2026/09/15
Chien Tzu-ChengChen Jia-YunLo Ko-HsuanFang Yi-WeiTsai Chia-ChiLiu Xu-ChenHsu Chian-JuChang Jen-JuiLou You-SyuanYin Yi-HsuanCheng Chih-ChengYu Hsin-HsienSu Bor-Chyuan - Cough is a prominent and often persistent manifestation of chronic bronchitis (CB) that is frequently difficult to resolve. While Qi Feng Gu Biao Granules (QFGBG) is a traditional Chinese medicine commonly used to treat CB, its pharmacological basis for CB-related cough remains unclear.This study characterized the chemical profile of QFGBG by UPLC-Q-TOF/MS, evaluated its antitussive and anti-inflammatory effects in a rat model induced by lipopolysaccharide instillation combined with cigarette smoke exposure, and integrated network pharmacology, molecular docking, Western blotting, and plasma metabolomics to explore the underlying mechanism.QFGBG reduced cough frequency, prolonged cough latency, improved body-weight gain, and decreased the lung index and wet-to-dry ratio. Histological analyses showed attenuation of lung and tracheal inflammatory injury and mucus hypersecretion. QFGBG also decreased the expression of inflammatory and cough-related factors. Network pharmacology identified 215 overlapping QFGBG-CB targets, with enrichment in inflammatory and metabolic pathways, including the AGEs/RAGE signaling pathway. Molecular docking suggested favorable binding of core components, including Formononetin, Acacetin, and Vanillin, to key targets. Western blotting confirmed that QFGBG downregulated AGEs, RAGE, p-STAT1/STAT1、p-STAT3/STAT3. Metabolomics indicated regulation of glycerophospholipid and arachidonic acid metabolism. These findings suggest that the active components of QFGBG may alleviate CB-related cough by inhibiting the AGEs/RAGE signaling pathway and regulating arachidonic acid and glycerophospholipid metabolism, thereby reducing pulmonary and neurogenic inflammation and the release of cough-related mediators. - Source: PubMed
Publication date: 2026/08/25
Fang FangGu YuanyuanLiu XinyuLiu XinyingWang YatingMeng YanliGuo YuyanZuo JunWang Weiming - Acquired resistance to osimertinib in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) arises from both tumor cell-intrinsic pathways and tumor microenvironmental cues. Cancer-associated fibroblasts (CAFs) are critical stromal components that drive therapeutic resistance, yet the complete molecular and metabolic cascade linking CAFs to EGFR downregulation and osimertinib insensitivity remains unclear. This work aimed to clarify how CAF-derived signals trigger epithelial-to-mesenchymal transition (EMT), lipid metabolic rewiring, and loss of EGFR expression to confer osimertinib resistance. - Source: PubMed
Publication date: 2026/09/29
Ye FeiWu JiabaoLiu DiLi YuhuiZhu NingChen Limin - Defensins are cysteine-rich innate immune effector peptides that support antimicrobial defense, immune regulation, and mucosal homeostasis. Because these activities occur within redox-sensitive environments, a functional relationship may exist between defensin biology and the thioredoxin (Trx)/thioredoxin-interacting protein (TXNIP) axis. The strongest direct evidence is Trx1-mediated reduction of human β-defensin 1 (hBD1), which enhances its antimicrobial activity. Accordingly, this review examines the redox-sensitive interfaces linking defensin-associated responses with the Trx1/TXNIP axis. Redox-sensitive interfaces examined in detail include TLR/NF-κB signaling pathways, dendritic cell maturation, nutrient-sensitive antimicrobial secretion, and IL-22/STAT3-dependent Paneth-cell responses. These relationships are subtype-, isoform-, species-, and model-specific, with varying degrees of direct and indirect support. These interactions may be particularly relevant in diseases involving epithelial stress, microbial imbalances, and dysregulated innate immune activation. A deeper understanding of these interfaces may provide insight into redox-based mechanisms controlling innate immunity and translational applications in inflammatory diseases. - Source: PubMed
Publication date: 2026/09/29
Dagah Omer M AUllah ZakirAlhameed Alaa Majeed MutasharAl-Azzani HamdiManzoor RakiaKhamis Mussa YussufLiu ZhenbaoLu Jun - Ulcerative colitis (UC) is driven by relentless mucosal inflammation and epithelial barrier compromise. Cyclin-dependent kinase 9 (CDK9) governs transcriptional elongation, yet its therapeutic potential in restoring the intestinal barrier via the STAT3 signaling axis remains underexplored. - Source: PubMed
Publication date: 2026/09/22
Zhao WencuiWu YanyunZhao NanZhang YanLiu LuZhang WeiZhao Qinglan