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
Ask about this productRelated 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
- Metabolic reprogramming within the tumor microenvironment is a pivotal barrier to effective immune checkpoint blockade (ICB). While programmed death ligand 1 (PD-L1) is well characterized as a ligand inhibiting T-cell function, its intrinsic 'reverse signaling' role in regulating tumor metabolism and shaping the immune landscape remains poorly understood. Here, we investigated the metabolic determinants of resistance to anti-programmed cell death protein 1 (anti-PD-1) therapy and the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/09/02
Lian WenxinYang HuiZhang YuqiLiu ChenchenFang ChunyaoXu MengyueYang YixingWang YanJiang RunqiuXu JingGao Wen - Dimethylcurcumin (ASC-J9), a derivative of curcumin, has been reported to possess anticancer activity. However, its potential impact on oral squamous cell carcinoma (OSCC) has not been fully characterized. In this study, we aimed to determine whether ASC-J9 inhibits OSCC metastasis and to elucidate the molecular mechanisms involved. Our findings indicate that ASC-J9 treatment significantly reduced OSCC metastasis both in vitro and in vivo. Notably, ASC-J9 treatment led to a marked decrease in both mRNA and protein levels of integrin beta 8 (ITGB8) in OSCC cells. In addition, ASC-J9 suppresses epithelial-mesenchymal transition (EMT) through the upregulation of E-cadherin and the downregulation of vimentin, fibronectin, Snail, and Slug expression. Moreover, ASC-J9 treatment led to a reduction in phosphorylated STAT3 (p-STAT3) levels. Activation of STAT3 by the selective activator colivelin reversed the ASC-J9-induced suppression of ITGB8 expression and cell migration. These findings suggest that ASC-J9 inhibits ITGB8 in OSCC cells by blocking STAT3 activation, thereby reducing their invasive and migratory capabilities. Collectively, our results support ASC-J9 as a promising therapeutic candidate for the treatment of OSCC. - Source: PubMed
Publication date: 2026/09/02
Chen Pei-NiLin Chiao-WenLai Chih-TingYang Shun-FaChang Yu-Chao - Tumor immune evasion is a pivotal mechanism driving therapeutic resistance and poor prognosis in lung cancer. The interleukin-20 receptor β subunit (IL20RB) is implicated in chronic inflammation and oncogenesis, but its precise function and molecular basis in non-small cell lung cancer (NSCLC) require elucidation. - Source: PubMed
Publication date: 2026/08/31
Wang YanghaoLi GuoyuWang WeizhouZhang HengruiZhang YuDeng YajieMu SirongYuan SiyuTu YulinNi JiayiHe YongwenBian Li - Recording and real-time imaging of promoter activities are critical for deciphering signaling cross-talk, but technologies for simultaneously capturing multiple transient events in living cells are lacking. Here, we design fluorescent protein-based ticker tapes (FPTT) for multiplexed, scalable, longitudinal recording of single-cell physiological activities by integrating multispectral monomeric fluorescent proteins with self-assembling protein fibers. FPTT logged dose-dependent, reversible endogenous cFos transcriptional histories in hippocampal neurons at 3-hour resolution over 8 days. We engineered FPTT variants for human nuclear factor κB (NF-κB), Janus kinase/signal transducer and activator of transcription 3 (STAT3), mechanistic target of rapamycin (mTOR), nuclear factor of activated T cells (NFAT), and adenosine 3',5'-monophosphate (cAMP) signaling. This expanded toolset enabled quantification of cFos and NF-κB cross-talk in neurons, tracking of STAT3/cAMP dynamics during mouse liver injury, discovery of unexpected NFAT/STAT3 cross-talk, and characterization of cell cycle-dependent oscillating mTOR dynamics. Last, we achieved simultaneous analysis of four major pathways during T cell activation. FPTT provides a versatile platform to investigate transcriptional histories and signaling interplay, with broad applications in developmental biology and disease modeling. - Source: PubMed
Publication date: 2026/09/02
Wang RuizhaoJiang JianLi ZhuoyuanLiu TianningWang YangdongXie MingqiPiatkevich Kiryl D - Acute kidney injury (AKI) affects a considerable proportion of patients that represents a major challenge for clinical treatment. Gut microbiota metabolites have been reported to attenuate acute kidney injury (AKI), yet their underlying mechanisms remain largely elusive. The present study aimed to explore the protective mechanisms of these metabolites against AKI using. - Source: PubMed
Publication date: 2026/09/02
Yao WeiguoHuo JinlinLiu KunTao Pengyu