Stat1 ELISA Kit
- Known as:
- Stat1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- EK1070
- Product Quantity:
- kit
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- Stat1 ELISA Kit
Related genes to: Stat1 ELISA Kit
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
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- The ten-eleven translocation (TET) family genes, which encode 5-methylcytosine (5mC) dioxygenases, play a "double-edged sword" role in tumor initiation and progression. However, the functional role and molecular mechanism of tumor cell-intrinsic TET3 in anti-tumor immunity remain incompletely understood. Here, we uncover that TET3 mRNA expression was aberrantly elevated in multiple cancer types and correlated with poor overall survival. Transcriptomic analysis reveals that TET3 depletion upregulated the expression of innate immune response genes, including numerous interferon-stimulated genes (ISGs), in cancer cells. The expression levels of dsRNA sensors (i.e., MDA5 and RIG-I) were increased in TET3 KO or KD cells, while the biogenesis of endogenous dsRNA was not affected. Mechanistically, TET3 regulates type I interferon signaling by inhibiting STAT1 activation. Importantly, depletion of TET3 in B16F10 melanoma cells significantly curbed the synergistic tumor growth, accompanied by increased tumor-infiltrating CD4 T cells, CD8 T cells, and dendritic cells. Notably, analysis of the TCGA dataset also shows that TET3 expression levels were negatively correlated with tumor-infiltrating cytotoxic CD8 T cells and MHC-I expression across multiple cancer types. Taken together, our findings identify TET3 as a new negative regulator of the type I interferon signaling in cancer cells. We envisage that targeting the tumor cell-intrinsic TET3 could reduce tumor immune evasion and promote anti-tumor immunity. - Source: PubMed
Publication date: 2026/04/29
Liu LuZhao WenxuanShang TianbaoXu BoWang MengyuanLi XinzeMin JieXu WenqiShen HongjieTan LiShi Yujiang Geno - Chronic mucocutaneous candidiasis (CMC) is a condition characterized by persistent or recurrent infections caused by candida species. Gain-of-function (GOF) mutations in signal transducer and activator of transcription-1 (STAT1) have been identified as a major cause of CMC and are linked to a broad clinical spectrum, including increased susceptibility to infections and vascular abnormalities. We present the case of aortic calcification in a patient with a STAT1 GOF mutation. The 8-year-old male patient had recurrent oral ulcers, upper respiratory tract infections, and pneumonia, and was found to have calcifications in the aortic arch and branches. Treatment with ruxolitinib led to significant clinical improvement, although no regression in aortic calcification was observed. STAT1 GOF mutations may enhance a pro-osteogenic environment through sustained activation of the Janus Kinase (JAK)-STAT pathway. This case highlights the potential link between STAT1 GOF mutations and vascular calcification and underscores the need for further investigation into the long-term vascular impact of JAK inhibition. - Source: PubMed
Publication date: 2026/04/15
Sonmez GamzeSelcuk Sinem NurHaliloğlu MithatCagdas Deniz - This study aimed to elucidate the role of ROS-related genes in esophageal squamous cell carcinoma (ESCC) prognosis and the cellular mechanisms involving FOXM1 and SESN2. A prognostic model incorporating six genes (FOXM1, SESN2, APOD, GATM, HEBP2, STAT1) was developed using three ESCC gene expression datasets via univariate Cox regression, LASSO-Cox algorithm, and multivariate validation. Functional assays revealed that FOXM1 knockdown elevated intracellular ROS and malondialdehyde (MDA) levels while reducing total glutathione and antioxidant capacity, impairing proliferation, migration, and cell cycle progression. RNA-seq and luciferase assays confirmed SESN2 as a transcriptional target of FOXM1. Dual knockdown of FOXM1 and SESN2 exacerbated oxidative stress, decreased mitochondrial membrane potential, and increased cell death, accompanied by mitochondrial morphological changes (reduced shrinkage, increased membrane density). Western blotting showed decreased BCL2 and GPX4 expression but increased LC3-II and -mTOR levels. These findings demonstrate that the FOXM1-SESN2 axis shields ESCC cells from oxidative stress, offering a rationale for future mechanistic investigations. - Source: PubMed
Publication date: 2026/05/05
Wu ZhishengZhang XiaonaChen MantongGao ChenmengZheng XiaoqiPeng ZhongteDu ZepengWu Bingli - The ability of Salmonella Typhimurium to exploit macrophages as a niche for survival, replication, and dissemination is central to its pathogenesis. The effector SteE, which polarizes macrophages into an anti-inflammatory state, is critical during invasive disease. SteE operates via an unprecedented mechanism, reprogramming the host serine/threonine kinase GSK3 to perform tyrosyl-directed phosphorylation of neosubstrates, including the immune transcription factors STAT1 and STAT3. Here, we demonstrate that SteE-driven transcriptional reprogramming relies critically and specifically on STAT3 phosphorylation and DNA binding. By activating STAT3 via a non-canonical pathway, bypassing endogenous negative feedback mechanisms, SteE drives hyperactivation of STAT3 target genes, surpassing the effects of canonical IL-10 signaling. Hyperactivation correlates with elevated phosphorylated STAT3 in the macrophage nucleus and coordinated chromatin remodeling at STAT3 target loci. Overall, our study illustrates how hijacking of a signaling pathway by SteE dramatically reshapes the macrophage gene regulatory network to enhance Salmonella immune evasion. - Source: PubMed
Publication date: 2026/05/08
Diaz-Del-Olmo InesO'Sullivan Paul AWilson Thomas SMajstorovic AndreaMiller GeorgiaShizukuishi SayakaStypulkowska AdrianaPanagi IoannaGrzymajlo KrzysztofOgawa MichinagaBezbradica Jelena SHill Peter W SThurston Teresa L M - Chronic lung allograft dysfunction (CLAD) significantly limits long-term survival of lung transplant recipients, with viral infections acting as critical contributors to its pathogenesis. The mechanisms linking viral infections to CLAD-associated airway fibrosis remain incompletely understood. This study investigates the role of the type I interferon (IFN) master regulator IRF7 in virus-induced airway fibrogenesis. - Source: PubMed
Publication date: 2026/05/08
Banday Mudassir MRahman MizanurGoda YasufumiPotter Andrew SNaito TatsuhikoMallidi HaripriyaSurolia RanuLee StefiRehman RakhshindaLoor GabrielHayes DonSharma Nirmal S