Ask about this productRelated genes to: RSAD2 antibody
- Gene:
- RSAD2 NIH gene
- Name:
- radical S-adenosyl methionine domain containing 2
- Previous symbol:
- -
- Synonyms:
- cig5, viperin, vig1
- Chromosome:
- 2p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-08
- Date modifiied:
- 2014-11-19
Related products to: RSAD2 antibody
Related articles to: RSAD2 antibody
- Porcine deltacoronavirus (PDCoV) is an emerging enteropathogenic coronavirus that causes severe diarrhea in swine industries worldwide. However, the interactions between PDCoV and host cells remain poorly understood. In this study, we employed transcriptomic and proteomic analyses to investigate host responses to PDCoV infection. Our results identified 1448 differentially expressed genes (DEGs) at 1.5 h post-PDCoV infection and 11,753 DEGs, along with 898 differentially expressed proteins (DEPs) at 18 h post-PDCoV infection. Furthermore, several signaling pathways, including innate immunity, autophagy, and ferroptosis, were primarily enriched following an integrated analysis of the transcriptome and proteome. Protein-protein interaction (PPI) analysis indicated that proteins closely associated with these pathways, such as interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), myxovirus resistance 2 (MX2), interferon-stimulated gene 15 (ISG15), radical S-adenosyl methionine domain containing 2 (RSAD2), 2'-5'-oligoadenylate synthetase like (OASL), autophagy related 14 (ATG14), and glutathione peroxidase 4 (GPX4), were central to the interaction network. Importantly, we demonstrated that autophagy and ferroptosis were induced upon PDCoV infection, and that inhibition of autophagy significantly suppressed the induction of PDCoV-induced ferroptosis, which decreases the viral proliferation. Overall, our findings provide a comprehensive overview of transcriptomic and proteomic changes following PDCoV infection and enhance the understanding of PDCoV pathogenesis, which will be beneficial for improving strategies for the prevention and control of PDCoV infection. - Source: PubMed
Publication date: 2026/05/18
Yang XiaozhuMi XingyuLiu WeiZainab FarwaWu MinruiYin HanweiLiu MengyuanZhang TingSun ZilongZhang DingTang PanSong TaoDuan LiqiangXi YiboWang ChenyangLi WeiWang HaidongYang Bo - The skin harbors a complex immune microenvironment that integrates innate and adaptive components and plays a critical role in vector-borne pathogen transmission. To investigate immune responses during tick-mediated transmission of Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV), we analyzed skin from BALB/c mice bitten by artificially infected Amblyomma testudinarium nymphs. Skin samples were collected at time points corresponding to peak viral RNA levels (days 6-7 post-attachment) and analyzed by transcriptomics, followed by real-time PCR and immunohistochemical (IHC) analyses. Transcriptomic analysis revealed increased expression of immune-related genes, particularly those associated with type I interferon signaling. Interferon-stimulated genes (e.g., Rsad2, Ifit family members) and monocyte-associated markers (e.g., Ly6c2) were elevated in RNA sequencing data, while real-time PCR analysis showed similar trends but did not reach statistical significance. IHC revealed colocalization of viral antigens with macrophages in the infected skin, as characterized by Iba1 expression. Further analysis demonstrated a higher density of Ly6c2-positive inflammatory monocytes, consistent with transcriptomic observations. In addition, BST2 (Tetherin) expression was increased, consistent with activation of a localized Type I IFN-mediated antiviral response. However, the strong inflammatory response induced by tick feeding may obscure infection-specific transcriptional changes at these later time points. Overall, our findings demonstrate that tick-mediated SFTSV infection was associated with interferon-related gene expression and recruitment of monocyte-lineage cells at the skin interface, while highlighting the complex interplay between viral infection and tick-induced host responses. - Source: PubMed
Publication date: 2026/05/18
Lau Alice C CMori HiroshiSakai YusukeShimoda HiroshiNagata NoriyoMatsumura TakayukiShimojima MasayukiToyoda AtsushiHayasaka DaisukeSuzuki TadakiEbihara HidekiTakano Ai - Patients with Systemic lupus erythematosus (SLE) who carry a high genetic burden often experience more severe disease. To understand the molecular consequences of polygenic risk, we analyzed single-cell gene expression profiles in SLE patients stratified by genetic risk. - Source: PubMed
Publication date: 2026/05/12
Sayadi AhmedEloranta Maija-LeenaOparina NinaWallgren MarcusSkoglund ElisabethFrodlund MartinaSjöwall ChristopherRönnblom LarsLeonard Dag - Transposable elements (TEs) are major contributors to genome plasticity and can reshape gene regulation through stress-responsive activation and the formation of TE-gene chimeric transcripts. Although therapeutic stress is known to perturb transcriptional networks in cancer cells, its impact on canonical TE transcription and TE-gene chimera formation in esophageal squamous cell carcinoma (ESCC) remains poorly defined. To address this, we performed a comprehensive transcriptome-wide analysis of TE expression and TE-gene chimeric transcripts in KYSE150 ESCC cells following combined 125I radiation and carfilzomib treatment. The TE analysis showed 148 dysregulated TEs, characterized by ERV1 LTR element enrichment and distinct treatment-control sample separation, indicating structured remodeling of the TE transcriptome. We identified 301 significant TE-gene chimeric events, indicating category-specific remodeling with an increase in TE-initiated and TE-exonic chimeras and a decrease in TE-terminal events. The TE families that underwent the most transcriptional changes were not those that drove chimeric events, indicating that global TE activation does not passively cause chimera remodeling. The gene repression was strongly associated with chimeric transcripts, and gene expression changes were negatively correlated with chimerism frequency. , , and , strongly downregulated genes, produced novel TE-derived isoforms and were high-potential functional candidates. Epigenetic context analysis showed considerable overlap between exonized chimeras and candidate cis-regulatory elements, suggesting a potential association with regulatory genomic contexts. Pathway enrichment analysis showed synchronized transcriptomic reprogramming and cell cycle and DNA repair pathway activation and autophagy inhibition. In esophageal cancer cells, concurrent genotoxic and proteotoxic stress causes complex TE remodeling, linking traditional TE transcriptional alterations to structured TE-gene chimera development and stress-related transcriptome reprogramming. - Source: PubMed
Publication date: 2026/04/13
Majid MuhammadMoeen MuhammadAmjad NoumanKhan HashimSun ZhaojianWu LinpingLi Zhiyuan - Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and hospitalization in infancy. Reliable biomarkers reflecting host antiviral responses and disease dynamics are still lacking. - Source: PubMed
Publication date: 2026/04/01
Galliano IlariaLiguori Stefania AlfonsinaPau AnnaMontanari PaolaCalvi CristinaClemente AnnaMassobrio AnnaLinari ClaudiaGambarino StefanoConio AlessandraBergallo Massimiliano