STAT1 Antibody
- Known as:
- STAT1 Antibody
- Catalog number:
- XW-8116
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- STAT1 Antibody
Related genes to: STAT1 Antibody
- 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
Related articles to: STAT1 Antibody
- Resistance to inhibitors (BRAFi), alone or with MEK inhibitors (MEKi), limits durable responses in -mutant melanoma. To characterize resistance-associated cell-state evolution, we analyzed 674 melanoma cells from six mice bearing tumors from a single patient-derived V600E-mutant melanoma xenograft (PDX) lineage before treatment, during initial regression, at minimal residual disease, and at resistant regrowth. Unsupervised clustering based on a -centered network feature set comprising 2506 candidate genes identified six transcriptional states, which were characterized using transcriptomic analyses. Cluster 4 was detected exclusively at resistant regrowth, a phase marked by MAPK pathway reactivation, and exhibited enhanced JAK-STAT/interferon signaling and increased , , , , and regulon activities. Network inference predicted - and - regulatory links, suggesting candidate routes to MAPK reactivation through overexpression and -mediated bypass signaling. External analyses partially recapitulated the resistance-associated transcriptional program in independent melanoma cell-line datasets and yielded limited, inconclusive evidence for the predicted - association in public perturbation datasets. Cluster 2 represented a pre-existing proliferative state whose signature was associated with shorter progression-free survival in pretreatment clinical cohorts. Together, these findings distinguish a therapy-associated acquired-resistance state from a pre-existing proliferative resistance-associated state and nominate the predicted - and - links for functional validation. - Source: PubMed
Publication date: 2026/09/09
Fu HaoWang MengyaoZhu HaiboLi WeihuaShen XiaopeiYan HaidanHe Jun - Herpes simplex encephalitis (HSE), predominantly caused by herpes simplex virus type 1 (HSV-1), is the most common sporadic viral encephalitis worldwide and remains life threatening despite antiviral therapy. Although herpes simplex virus (HSV) infection is highly prevalent, only a minority of individuals develop HSE, highlighting the critical contribution of host-specific factors to disease susceptibility. This review summarizes current knowledge regarding HSE epidemiology, antiviral immunity, genetic susceptibility, and therapeutic advances. Underlying inborn errors of immunity fall into three mechanistic groups: impaired innate immune sensing pathways, including Toll-like receptor 3 (), retinoic-acid-inducible gene-I ()/melanoma differentiation-associated gene 5 (), and cyclic GMP-AMP synthase ()-stimulator of interferon genes (STING), which compromise type I interferon (IFN) production in central nervous system (CNS) resident cells; disrupted neuron intrinsic antiviral mechanisms represented by mutations in specific genes (e.g., , , and ); and defects in other IFN signaling molecules, including interferon-α/β receptor 1 () and 2 (), as well as signal transducer and activator of transcription 1 () and 2 (), which further weaken antiviral defenses. These findings underscore cell autonomous antiviral responses within the brain and provide insights into the selective vulnerability to HSE. Emerging therapeutic strategies aim to integrate antiviral treatment with modulation of host immune responses and, potentially, personalized approaches based on genetic profiling. In all, we emphasize the pivotal role of CNS-intrinsic immunity and host genetic factors in shaping disease outcomes. A deeper understanding of the interplay between HSV and host defense mechanisms will facilitate the development of improved diagnostic tools and targeted therapies, ultimately reducing the burden of this devastating disease. - Source: PubMed
Publication date: 2026/09/18
Zhan YufeiLi JingYuan QiaolingYin XianzhengTong Jie - Long non-coding RNAs (lncRNAs) are regulatory RNA molecules involved in numerous biological processes, including immune response. Although their functions remain difficult to characterize, lncRNAs have been associated with both productive and immune traits in pigs. Because immune parameters have been proposed as indicators of immunocompetence, studying lncRNA regulation in immune-related tissues may contribute to improving pig robustness and disease resistance. In this study, whole-blood RNA-seq data from 255 commercial 60-day-old Duroc pigs were used to identify lncRNA-associated immune mechanisms. Co-expression networks were constructed from highly correlated lncRNAs and other genes, followed by functional enrichment analyses. Associations between network genes and 15 immune-related phenotypes were evaluated, and putative RNA-RNA interactions were characterized. The largest network identified was enriched for immune pathways, particularly antiviral response, and included key transcription factors such as , , , and . Four genes within this network (, ENSSSCG00000036342, , and ) were in silico predicted to interact with the same domain of lncRNA ENSSSCG00000055468. Additional networks were associated with V(D)J recombination, cytokine-mediated signalling, and other immune functions. A second putative RNA-RNA interaction was identified between lncRNA ENSSSCG00000058144 and . These findings reveal potential lncRNA-mediated regulatory mechanisms underlying porcine immunity and provide candidate RNA-RNA interactions that require future validation. - Source: PubMed
Publication date: 2026/09/17
Jové-Juncà TeodorHernández-Banqué CarlesCrespo-Piazuelo DanielGonzález-Rodríguez OlgaQuintanilla RaquelBallester Maria - African swine fever virus (ASFV) pA137R is a key immune evasion protein known to target TBK1 and suppress the cGAS-STING pathway; however, whether it modulates type I interferon (IFN) signal transduction remains unknown. In this study, we investigated the role of the A137R protein (pA137R) in the JAK-STAT type I IFN signaling cascade. We found that pA137R directly interacts with TYK2 via a 10-amino-acid motif (aa81-90), interferes with the IFNAR1-TYK2 interaction. This disruption inhibited the phosphorylation and nuclear translocation of both STAT1 and STAT2, leading to a pronounced suppression of interferon-stimulated gene (ISG) expression. Consistently, an A137R-deleted ASFV strain displayed markedly enhanced sensitivity to IFN stimulation and produced significantly higher levels of ISGs compared to the parental virus. Collectively, these findings identify pA137R as a potent antagonist of the JAK-STAT pathway that, by targeting TYK2, blocks STAT1/2 activation and ISG induction. This work reveals a previously unrecognized mechanism by which this virulence factor disarms type I IFN-mediated innate antiviral responses and, together with its known activity against cGAS-STING, underscores the pivotal role of A137R in ASFV immune evasion. - Source: PubMed
Publication date: 2026/09/15
Wu ZongyiShao HongxiaButaye PatrickChen HongjunQin AijianQian Kun - Lymph node metastasis in esophageal squamous cell carcinoma (ESCC) is associated with poor prognosis, and screening for potential biomarkers of metastasis is significant for improving the prognosis of ESCC. After batch effect removal and integration of two ESCC transcriptome datasets (GSE157804, GSE118493), differentially expressioned gene analysis was performed. The intersection of differentially expressed genes was obtained to identify characteristic genes associated with lymph node metastasis in ESCC. GO/KEGG enrichment analyses were conducted for the characteristic genes. The top 10 pathways and pathway genes based on q-value were selected to construct a PPI network. Hub genes were identified and intersected with the characteristic genes to determine key genes. GO/KEGG enrichment, expression level analysis, and immune infiltration analysis were performed for the key genes. Immunohistochemistry was used to validate the expression levels of key genes in clinical samples. A cell model with regulated expression of key genes was established to verify their impact on the invasive and migratory capabilities of ESCC cells and epithelial-mesenchymal transition (EMT), as well as ECM‑related gene expression. A total of 542 characteristic genes associated with lymph node metastasis in ESCC were identified through differential gene analysis, which were mainly enriched in extracellular matrix-related pathways. PPI network analysis identified 63 hub genes, and the intersection with characteristic genes resulted in 20 key genes, which were also primarily enriched in extracellular matrix-related pathways. Expression level analysis showed that key genes such as STAT1, STAT2, IFIT1, and IFIT3 were highly expressed in metastatic ESCC tissues compared to primary sites and adjacent non-tumor tissues. Immune infiltration analysis revealed a significant positive correlation between IFIT3, STAT1, STAT2, and M1 macrophage polarization. Immunohistochemical analysis indicated high expression of STAT1 in ESCC patient samples with lymph node metastasis. Upregulation of STAT1 in ESCC cells enhanced cell invasion, migration, EMT levels and ECM‑related gene expression, while downregulation of STAT1 expression suppressed these processes. Consistently, an additional gain‑of‑function experiment further confirmed these promoting effects. STAT1 serves as a biomarker for lymph node metastasis in ESCC. The expression level of STAT1 is positively correlated with the degree of lymph node metastasis in ESCC clinical samples. Overexpression of STAT1 promotes the invasion, migration, EMT and ECM‑related gene expression of ESCC cells, while the downregulation of STAT1 inhibits these effects. - Source: PubMed
Publication date: 2026/09/05
Lv GuoliLi HaoyuLei YoumingPeng JungaoLiu FanghaoZhao Wei