STAT4 Antibody
- Known as:
- STAT4 Antibody
- Catalog number:
- XW-8119
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- STAT4 Antibody
Related genes to: STAT4 Antibody
- Gene:
- STAT4 NIH gene
- Name:
- signal transducer and activator of transcription 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q32.2-q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2018-02-13
Related products to: STAT4 Antibody
Related articles to: STAT4 Antibody
- Emerging evidence underscores the pivotal role of CD4 effector T cells in antitumor immunity, yet their full therapeutic potential remains underexplored. This study investigates the impact of targeting the Wnt coactivators B-cell lymphoma 9 and B-cell lymphoma 9-like (BCL9/BCL9L) on CD4 T cell-mediated antitumor immunity. We demonstrate that either genetic deletion or pharmacological inhibition of BCL9/BCL9L suppresses tumor progression and increases CD4 T cell activation in the tumor microenvironment (TME). Critically, loss of Bcl9/Bcl9l skews CD4 T cell differentiation toward a Th1 phenotype at the expense of Th2, Th17, and Treg lineages, thereby establishing a Th1-dominant TME and unleashing a direct cytotoxic program in these Th1 cells. Mechanistically, BCL9/BCL9L inhibition promotes Th1 polarization by suppressing TCF4-mediated regulation of PIAS family genes and enhancing STAT1/STAT4 activation, thereby driving a potent Th1-mediated antitumor response. Collectively, our findings identify BCL9/BCL9L as critical negative regulators of CD4 T cell antitumor immunity and establish them as promising therapeutic targets for reprogramming the TME toward a Th1-supportive state. - Source: PubMed
Publication date: 2026/06/29
Zhu Yuan-YuanLi An-QiYang FanDong Yu-XuanHuang Ya-SiMeng Xiang-JingZhang Dai-ZhouLi YeXian Yan-FangZhu DiFeng Mei - Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced non-small cell lung cancer (NSCLC). However, the limited predictive value of PD-L1 expression as a biomarker underscores the urgent need for more reliable predictors of ICI response. Interferon regulatory factor 1 (IRF1) is a transcription factor that lies downstream of interferon-γ signaling and directly regulates (PD-L1) transcription. Here, we performed a comprehensive bioinformatic analysis to identify microRNAs (miRNAs) that may be associated with expression in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Using data from The Cancer Genome Atlas (TCGA), we identified 20 miRNAs whose expression levels consistently and negatively correlated with IRF1 mRNA levels in both LUAD and LUSC. Among these, only hsa-miR-301b possesses conserved binding sites in the 3'UTR of IRF1 mRNA, suggesting direct post-transcriptional repression. For the remaining 19 miRNAs, we hypothesized an indirect mechanism of action. Further analysis revealed that hsa-miR-183 and hsa-miR-141 may target the transcription factor genes and , respectively, both of which positively correlate with expression and are themselves associated with improved survival in ICI-treated patients. This study delineates a multi-layer miRNA regulatory network associated with expression in NSCLC and identifies hsa-miR-301b, hsa-miR-183 and hsa-miR-141 as candidate upstream regulators of . Direct survival analysis for these miRNAs in ICI-treated cohorts was not feasible due to the lack of publicly available miRNA-seq data with treatment annotations; therefore, their clinical predictive value remains hypothetical, and experimental validation is required to assess their potential as predictors of ICI response. - Source: PubMed
Publication date: 2026/06/08
Karaseva Dariya VPerevalova Alina MKalinina Tatiana SKononchuk Vladislav VKozlov Vadim VGulyaeva Lyudmila FPustylnyak Vladimir O - Selective immunoglobulin A deficiency (IgAD) is the most prevalent primary immunodeficiency and frequently coexists with autoimmune diseases (ADs), suggesting a shared genetic etiology. While genome-wide association studies (GWAS) have identified only a few risk loci for IgAD and hundreds for ADs, systematic cross-trait analyses are lacking, leaving the shared genetic architecture and underlying mechanisms poorly understood. In this study, we analyzed summary statistics from large-scale GWAS of IgAD and 10 common ADs. Cross-trait GWAS meta-analysis identified 51 pleiotropic loci significantly associated with IgAD and at least one AD (p < 5×10⁻⁸), 31 of which were novel for IgAD. Colocalization analysis further supported 33 shared loci between IgAD and ADs, including 19 novel IgAD loci, such as those near TNFAIP3, CD28, IRF4, STAT4, SH2B3, APOBR and RAD51B. Gene-level analysis revealed shared pathways involved in T-cell differentiation and the intestinal immune network for IgA production. Tissue heritability analysis identified whole blood and the intestine as critical tissues, while single-cell RNA sequencing (scRNA-seq) highlighted B cell subtypes in the peripheral blood and gut as the most affected cell types in IgAD and ADs. Mendelian randomization further demonstrated bidirectional causal relationships between IgAD and several ADs. Our findings reveal a shared genetic architecture between IgAD and ADs, highlighting common functional mechanisms and providing insights into their biological interplay and potential immune-based therapies. - Source: PubMed
Publication date: 2026/06/22
Dang XiaoWang Frank QingyunZhang CaicaiSu HuidongLei YaoYang JingLau Yu LungYang Wanling - Atherosclerosis represents a major risk factor contributing to the development and advancement of cardiovascular diseases. The present study aimed to investigate the role of impaired autophagy and mitochondrial dysfunction in THP‑1 macrophages induced by oxidized low‑density lipoprotein (ox‑LDL), a key factor in atherosclerosis and cardiovascular disease. The molecular mechanism underlying the contribution of ox‑LDL to macrophage dysfunction is poorly understood. The present study aimed to determine whether β‑hydroxybutyrate (BHB) protects autophagic and mitochondrial function in THP‑1 macrophages exposed to ox‑LDL. Using cell culture, western blotting, autophagy detection assay and measurement of mitochondrial membrane potential, the present study evaluated the effect of BHB on autophagic flux and mitochondrial integrity. Ox‑LDL treatment markedly increased p62 protein levels and decreased LC3‑II/LC3‑I ratios, indicating impaired autophagy. BHB decreased p62 levels, increased LC3‑II/LC3‑I ratios and restored autophagic flux (shown by increased autophagosome numbers) and improved mitochondrial membrane potential. In addition, BHB downregulated STAT4, which was upregulated by ox‑LDL, suggesting a signaling pathway through which BHB exerts its protective effect. The present findings demonstrate that BHB enhances autophagic activity and mitochondrial function in THP‑1 macrophages under ox‑LDL stress, highlighting its potential as a novel therapeutic agent for metabolic and cardiovascular disease. Future studies should examine in vivo applications and the broader implications of BHB in atherosclerosis. - Source: PubMed
Publication date: 2026/06/19
Luo WeiguangHe MeiWang Huiling - Natural killer (NK) cells are innate lymphocytes that rapidly respond to inflammatory cytokines during infection, but the mechanisms underlying such swift responses remain incompletely understood. Here, we investigated the RNA polymerase II (Pol II) dynamics during rapid cytokine-induced activation in NK cells. Brief exposure to the proinflammatory cytokine interleukin-12 (IL-12) elicited rapid, genome-wide redistribution of Pol II within minutes, with increased promoter-proximal Pol II pausing at effector loci including Ifng. This IL-12-induced Pol II reorganization was mediated by the transcription factor STAT4. We further identified the RNA helicase DDX5 as a STAT4 interaction partner required for optimal IFN-γ production and appropriate modulation of Pol II occupancy following IL-12 stimulation. Together, these findings identify STAT4/DDX5-mediated regulation of Pol II as a critical mechanism enabling the rapid responsiveness of NK cells to proinflammatory cytokines. - Source: PubMed
Publication date: 2026/06/18
Kim HyunuGrassmann SimonWong WilfredAdams Nicholas MKanno YukaO'Shea John JLeslie Christina SRogatsky InezSun Joseph C