Phospho STAT_1 (Tyr727) pAb
- Known as:
- Phospho STAT_1 (Tyr727) pAb
- Catalog number:
- ASAKAP-TF021D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Phospho STAT_1 (Tyr727) pAb
Related genes to: Phospho STAT_1 (Tyr727) pAb
- 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: Phospho STAT_1 (Tyr727) pAb
Related articles to: Phospho STAT_1 (Tyr727) pAb
- Perfluorooctanoic acid (PFOA), a major persistent per- and polyfluoroalkyl substance (PFAS), remains ubiquitous in humans, including pregnant women, despite regulatory actions to limit its production and use. The placenta has been proposed as a target of PFOA, however, the underlying mechanisms remain poorly defined. We exposed primary human placental cytotrophoblasts (CTBs) isolated from three second-trimester placentas to PFOA (0.1-25 μM) for 48 h. SWATH-MS identified 3,240 proteins, 274 of which were differentially expressed. Proteins involved in lipid and amino acid metabolism and innate immunity pathways were significantly enriched among these targets. Integration of protein and mRNA data sets revealed key molecules linking PFOA exposure to altered immune defense and placental dysfunction. Molecular docking and dynamic simulations predicted that PFOA and other PFAS directly interact with master regulators, including peroxisome proliferator-activated receptors α and γ (PPARα, PPARγ) and novel targets such as signal transducer and activator of transcription 1/2 (STAT1, STAT2) and interferon regulatory factor 1/3 (IRF1, IRF3). Benchmark modeling indicated that significant protein-level changes can occur at concentrations relative to reported serum concentrations and associated with placental toxicity in rodents. We propose that PFOA and other PFAS directly interact with these candidate regulators, contributing to placental dysfunction. - Source: PubMed
Publication date: 2026/06/10
Wang MengjingChen HaoKapidzic MirhanGormley MatthewTuomivaara SamiGutierrez Amanda MLi LinChen JessicaAbrahamsson Dimitri PHall StevenAlmeida Nuno M SSoshilov Anatoly AWoodruff Tracey JFisher Susan JRobinson Joshua F - Alphaviruses, including significant human pathogens like Chikungunya (CHIKV), Venezuelan Equine Encephalitis (VEEV), and the model Sindbis virus (SINV), pose a considerable global health threat. Their ability to establish infection and cause disease is critically dependent on successfully subverting the host's innate immune defenses, particularly the Type I Interferon (IFN-I) system. This review provides a comparative analysis of the molecular strategies employed by CHIKV, VEEV, and SINV to dismantle these antiviral pathways. We first outline the conserved principles that form a core alphavirus "toolkit" for evasion, such as the formation of membrane-bound replication factories to shield viral RNA from cytosolic sensors and NSP1-mediated mRNA capping to mimic host transcripts. The review then delves into the divergent, virus-specific tactics, highlighting the central role of the non-structural protein 2 (NSP2) as a master antagonist. We contrast the aggressive strategies of pathogenic alphaviruses-such as CHIKV NSP2-mediated cleavage of MAVS and degradation of STAT2, and VEEV-induced degradation of STAT1-with the more subtle, modulatory approach of SINV, which relies more on a global shutdown of host gene expression. These distinct molecular mechanisms are directly correlated with their varying pathogenic outcomes. Furthermore, we examine the remarkable adaptability of these strategies between vertebrate hosts, where suppressing the IFN system is paramount, and invertebrate vectors, where evading the RNAi pathway is the primary challenge. A comprehensive understanding of these commonalities and divergences in immune evasion is essential for the rational design of broad-spectrum antiviral therapeutics and next-generation vaccines. - Source: PubMed
Feyzi KambizMousavi Fatemeh SadatAbbasi Samaneh - Lipid droplets (LDs), once viewed as inert lipid storage sites, are now recognised as dynamic organelles central to cellular signalling and immunity. This study presents a dual-omics approach, integrating proteomics and lipidomics, to investigate LDs in the host antiviral response. In vivo and in vitro RNA viral infection models demonstrate that LDs rapidly remodel both their proteome and lipidome. The antiviral proteins RIG-I, MDA5, STAT1, STAT2, and viperin are specifically recruited to virus-induced LDs. Simultaneously, the LD lipidome shifts toward enrichment in long-chain polyunsaturated fatty acids and bioactive phospholipids, likely enhancing membrane dynamics and protein recruitment. Correlation analysis of matched proteomic and lipidomic datasets revealed extensive lipid-protein co-regulation on LDs and identified distinct correlation networks in which immune and antiviral proteins preferentially aligned with neutral lipid species. Enzymes involved in lipid metabolism and post-translational modifications are also upregulated, suggesting a mechanistic link between lipid remodeling and protein localisation. Functional assays utilizing artificial LDs revealed that arachidonic-acid and eicosapentaenoic-acid suppress viral replication and enhance type I and III interferon responses. These findings position LDs as key immunometabolic platforms in early antiviral defence. - Source: PubMed
Publication date: 2026/06/05
Monson Ebony ATelikani ZahraLaws Jay LMilligan Abbey JAmarasinghe IrumiBamford Sarah ERozario Ashley MSmith Monique LTran VivianDinh Quynh NWilliamson NicholasMechler AdamLiu BoyinJohnson Chad JPigram Paul JLeeming MichaelNie ShuaiHolien Jessica KHofer Markus JWhelan Donna RHelbig Karla J - Re Du Ning (RDN) injection is a modern Chinese herbal formulation with heat-clearing, wind-dispersing, and detoxifying properties. It is clinically used for the treatment of influenza-related high fever and upper respiratory tract infections, with validated clinical efficacy and a favorable safety profile. Although its anti-inflammatory activity has been extensively documented, the antiviral effects of RDN against influenza A virus (IAV) remain controversial, and the underlying mechanisms are not fully elucidated. - Source: PubMed
Publication date: 2026/06/02
Ke SiyuanChen RuonanWang JiaxiBi XiaozhaoZhang DajieLiu YeChen ZinuoLiu YuGeng Zikai - 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