STAT1 Antibody (Ab_727), pAb, Rabbit
- Known as:
- STAT1 Antibody (Ab_727), pAb, Rabbit
- Catalog number:
- A00454
- Product Quantity:
- 200ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- STAT1 Antibody (Ab_727) pAb Rabbit
Related genes to: STAT1 Antibody (Ab_727), pAb, Rabbit
- 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
- Gene:
- STAT2 NIH gene
- Name:
- signal transducer and activator of transcription 2
- Previous symbol:
- -
- Synonyms:
- STAT113
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT1 Antibody (Ab_727), pAb, Rabbit
Related articles to: STAT1 Antibody (Ab_727), pAb, Rabbit
- Sepsis has a high mortality rate, yet the cellular heterogeneity and transcriptional regulatory programs associated with divergent clinical outcomes remain incompletely understood. Here, we integrated two peripheral blood single-cell RNA-seq cohorts to explore prognosis-associated immune remodeling patterns in sepsis. Using reference-based annotation, pySCENIC-inferred regulon activity, pathway enrichment, and CellChat based ligand-receptor inference, we observed broad differences in cell composition, transcriptional programs, and intercellular communication between survivors and non-survivors. Non-survivors exhibited relative decrease of monocytes, B-cells, NK cells, and CD4/CD8 T cells, together with relative platelet expansion. cDC2 and plasmablasts showed relatively large transcriptional disturbance compared to other cell types. In cDC2, poor outcome was associated with increased TNF-α and NF-κB related regulon activity, which linked to AP-1 transcription factors (JUN, FOSL2, CEBPB, NFIL3, KLF6, and FOSB), together with reduced STAT1 and STAT2-associated interferon signaling. Gene regulatory network analysis highlighted cell type-specific transcription factor and target gene relationships. CellChat suggested that cDC2 may occupy a more connected position in survivors, whereas connectivity appeared reduced in non-survivors. Independent bulk transcriptomic validation supported increased FOSL2 and CEBPB expression, and a multivariable eight-transcription-factor model showed preliminary discriminatory performance. Overall, this study suggests that poor-outcome sepsis may be associated with altered cDC2 regulatory states and reduced cDC2 centered intercellular coordination. - Source: PubMed
Publication date: 2026/05/29
Yang YuanmingHua YiweiYang SuyiLiu NanLi Jun - Lambda interferons signal through the interferon lambda receptor-1 (IFNLR1) and IL10RB heterodimer to induce interferon stimulated genes (ISGs). We previously showed that proteins derived from distinct IFNLR1 splice isoforms uniquely influence gene expression and HBV replication in stem cell-derived hepatocytes (iHeps). Here, we evaluated signal transduction mechanisms of full-length IFNLR1 (variant 1) and a truncated variant missing part of the cytoplasmic JAK1-interacting domain (variant 2). - Source: PubMed
Publication date: 2026/05/29
Novotny Laura AMartinez-Morant CarlaDuncan Stephen ATraktman PaulaGooz MonikaMeissner Eric G - : The STAT (Signal Transducer and Activator of Transcription) family of seven transcription factors mediates cytokine and growth-factor signaling, regulating proliferation, differentiation, and immunity. While STAT3/STAT5 are established oncogenes and STAT1/STAT2 are classically viewed as tumor suppressors, emerging evidence indicates context-dependent roles in tumorigenesis. This study aimed to integrate evolutionary analysis with bulk transcriptomic, regulon, single-cell, and exploratory chromatin-binding analyses of the STAT family in human solid tumors. : Orthologs and paralogs of human STAT genes (81 sequences total) were retrieved across vertebrates and invertebrates; a phylogenetic tree was constructed using MUSCLE alignment and Neighbor-Joining in MEGA12. Differential expression was assessed in TCGA solid tumors versus GTEx normal tissues. Master-regulator activity was inferred using the algorithm. Single-cell RNA-seq datasets were used to compare malignant and non-malignant cell populations. STAT1 chromatin binding was examined via ChIP-seq in interferon-stimulated HeLa and K562 cells. : Phylogeny resolved seven conserved vertebrate clades, with endocrine-responsive STAT3/STAT5 showing higher conservation and immune-associated STAT1/STAT2/STAT4/STAT6 exhibiting faster divergence. The majority of STAT genes were frequently upregulated across multiple solid tumors, with activated regulons confirming functional transcriptional engagement. Single-cell analysis demonstrated tumor-cell-autonomous upregulation of STAT1 and STAT2 in the HNSCC dataset. STAT1 ChIP-seq revealed asymmetric forward/reverse-strand read density around peak summits, supporting non-canonical DNA recognition. : The STAT family operates as an evolutionarily conserved, broadly activated transcriptional module in human solid cancers, combining quantitative upregulation with qualitative shifts in DNA-binding dynamics. These findings refine our understanding of JAK/STAT signaling in oncology and highlight opportunities for network-targeted therapies. - Source: PubMed
Publication date: 2026/05/03
Lukic DunjaGuzzi Pietro HiramGiorgi Federico Manuel - Mycobacterium bovis bacillus Calmette-Guerin (BCG) is a form of live attenuated M. bovis-based vaccine used to prevent tuberculosis and other mycobacterial infections. BCG immunization also provides cross-protection against a broad range of viral pathogens. Recent studies show that a coordinated induction of innate and adaptive immune responses is involved, though the mechanisms are less defined. To investigate the cross-protection of BCG against virus infection, we used a mouse model of respiratory syncytial virus (RSV) infection and demonstrated that systemic administration of live BCG altered chromatin accessibility for transcriptional factor expression favoring Th1 response. Specifically, BCG-IV immunization protected mice against RSV infection. BCG immunization caused metabolic reprogramming in monocytes and neutrophils and innate immune response, leading to IL12/IL12R-mediated naïve CD4 T cell differentiation to the Th1 cell population. Integrated analysis of chromatin openness and transcriptomic data revealed that BCG administration upregulated transcription factors including interferon regulatory factors (IRF1) and signal transducer and activator of transcription (STAT1 and STAT2), a signature for interferon signaling and antiviral response. This work highlights a crucial role for the adaptive immune response in mediating naïve CD4 T cell differentiation and cross-protection through epigenetic remodeling for antiviral response against pathogens in an antigen-agnostic manner. - Source: PubMed
Publication date: 2026/05/16
Wang RuilinZhao YuanhuiYang JieLuo RenjieSun WeikangZhang MengyuLiu XiangdongHou YayiCao PengLi Erguang - Porcine epidemic diarrhea virus (PEDV) continues to pose a global threat to the swine industry, causing fatal neonatal diarrhea with a mortality rate approaching 100%. Currently, no effective targeted drugs have been approved. The coronavirus main protease (M), a conserved enzyme essential for viral replication, represents a promising target for antiviral development. Here, we demonstrate that Closantel, an FDA-approved veterinary drug, acts as a potent pan-coronavirus M inhibitor via enzymatic inhibition assays. Moreover, Closantel potently suppresses PEDV replication in Vero-E6 and IPEC-J2 cells, with EC values of 1.49 ± 0.38 μM and 4.32 ± 0.53 μM, respectively, and exhibits minimal cytotoxicity. Remarkably, Closantel triggers interferon secretion and activates JAK-STAT signaling pathways via phosphorylation of STAT1 and STAT2, establishing a dual antiviral mechanism. In summary, Closantel holds promise as a potential lead compound for developing targeted therapies against PEDV infection. - Source: PubMed
Publication date: 2026/05/12
Zhang LeiWang ZhuoyaXu FengLin Yuxi