Ask about this productRelated genes to: RSAD2 Blocking Peptide
- 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 Blocking Peptide
Related articles to: RSAD2 Blocking Peptide
- Axillary lymph node (LN) metastasis significantly impacts breast cancer (BC) prognosis. The role of the systemic immune environment in promoting metastasis remains unclear. - Source: PubMed
Chen BoMa KangWang YunjieZhang LiuluFeng XinyueLong ChengTan XuejingWang Kun - Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease with complex molecular mechanisms. Although transcriptomic studies have revealed prominent interferon signatures in SLE, robust prioritization of candidate genes across independent cohorts remains challenging. In this study, we performed a multi-cohort transcriptomic analysis using publicly available GEO datasets. Differential expression analysis was conducted independently within each cohort to minimize cross-study confounding. Machine learning models, including LASSO, support vector machine, and random forest, were applied for feature prioritization in a designated training cohort, followed by independent validation in separate datasets. Model interpretability was assessed using SHAP analysis. Immune cell composition was estimated descriptively using CIBERSORT. In addition, molecular docking and molecular dynamics simulations were performed as exploratory in silico analyses to evaluate potential protein-compound interactions. A set of consistently dysregulated genes across cohorts was identified, many of which are associated with interferon signaling. Among these, RSAD2 showed robust prioritization across multiple machine learning models. The predictive performance of the models was stable in independent validation datasets. SHAP analysis highlighted the contribution of interferon-stimulated genes to model predictions. Immune deconvolution suggested altered immune cell composition in SLE samples, consistent with previously reported immune activation patterns. Exploratory in silico analyses suggested a potential interaction between artemisinin and RSAD2. This study provides a robust, multi-cohort computational framework for prioritizing candidate genes associated with SLE. The findings highlight interferon-associated transcriptional features as reproducible molecular signatures of SLE and generate testable hypotheses for future experimental and clinical investigation. - Source: PubMed
Publication date: 2026/06/08
Apaer AishanjiangAobulitalifu AlimijiangKeyoumu JumahongAlifu AdilijiangAikebaier AlimuHasimu MilikanmuShi YanyanSulitan Maierhaba - Occupational noise-induced hearing loss (NIHL) is a common occupational disorder, yet non-invasive molecular indicators of chronic occupational noise exposure remain insufficiently characterized. Although the cochlear mechanisms behind NIHL have been extensively studied in experimental models, peripheral blood transcriptomic alterations in affected human populations are less well defined. In this exploratory study, we aimed to describe peripheral blood gene expression patterns associated with occupational NIHL and to generate candidate molecular signals for future validation. Peripheral blood RNA sequencing (RNA-seq) was performed in 11 male individuals with occupational bilateral sensorineural hearing loss and four noise-unexposed healthy male controls. Transcript abundance was quantified using a standardized RNA-seq workflow, and formal differential expression analysis was conducted on gene-level count data derived from Salmon quantification using DESeq2 with Benjamini-Hochberg correction. Through our analysis, we identified a limited set of differentially expressed genes, including upregulated interferon-associated transcripts, such as , , , and , host-defense-related genes, including , , and , and immune-regulatory transcripts such as and , together with downregulated non-coding RNAs including and . These findings suggest that occupational NIHL may be accompanied by detectable peripheral blood transcriptomic alterations, predominantly involving immune- and host-defense-related pathways. Given the limited cohort size and exploratory design, these genes represent preliminary candidates for validation in larger independent cohorts. - Source: PubMed
Publication date: 2026/05/08
Öztan Gözdeİşsever HalimGüldiken YahyaCanbaz SevgiOğuz FatmaKurt Özlem Karİşsever Tuğçe - : Gaucher disease (GD) arises from pathogenic variants in the gene and is known for its wide range of clinical presentations-a variability that genotype alone cannot adequately account for. : This study aimed to explore transcriptomic factors that might help explain why two genetically identical twins with type 1 GD developed noticeably different clinical outcomes. : We isolated peripheral blood mononuclear cells from both twins and two age-matched controls, then differentiated them into macrophages in vitro before conducting RNA sequencing. Gene expression differences were analyzed using established bioinformatics pipelines, and a subset of genes were subsequently assessed by quantitative real-time PCR (qRT-PCR) to confirm the sequencing findings. : Both twins shared a GD-associated transcriptional signature broadly reflecting immune activation and lysosomal stress. Interestingly, the twin who experienced systemic complications had a relative enrichment of interferon-responsive transcripts, while the less severely affected twin showed more pronounced suppression of small nucleolar RNA clusters. That said, neither difference held up after correcting for multiple comparisons, so these patterns are best viewed as exploratory trends rather than definitive findings. The qRT-PCR results lend partial support to this picture: stress- and immune-related genes (, , ) trended toward higher expression in patients versus controls, and interferon-stimulated genes (, , ) were more elevated in M2 than in M1. : Taken together, these findings suggest that factors beyond genetics-whether epigenetic, environmental, or otherwise-may play a meaningful role in shaping how GD manifests differently even between individuals with identical DNA. Although the data are preliminary, they point to transcriptomic profiling, paired with targeted validation, as a useful starting point for building hypotheses about why this disease looks so different from one patient to the next, even when the underlying mutation is the same. - Source: PubMed
Publication date: 2026/04/29
İnci AslıAydoğdu Demirel SümeyyeErgin Filiz Başak CengizBiberoğlu GürselOkur İlyasEzgü Fatih SüheylTümer LeylaÖktem Rıdvan MuratDökmeci Serap - The small-molecule pyridazinone derivative IMB5036 (IMB) exhibits significant cytotoxicity against multiple cancer cell lines, and KH-type splicing regulatory protein (KSRP) is confirmed as its direct binding partner. However, KSRP's functional role in neuroblastoma (NB) and the mechanism mediating IMB's antitumor effects remain unclear. This study analyzed public tumor databases and found KSRP expression negatively correlates with NB patients' median survival. Experiments showed IMB induces NB cell pyroptosis, immunogenic cell death (ICD, with calreticulin exposure), and cGAS-STING activation (to boost antitumor immunity), while CRISPR-Cas9-mediated KSRP knockout notably attenuates these effects. Transcriptome sequencing further confirmed KSRP mediates IMB's regulation of HSPA6/RSAD2. This study clarifies KSRP-dependent ICD drives NB antitumor immunity, providing a basis for KSRP-targeted NB immunotherapies. - Source: PubMed
Publication date: 2026/05/26
Dong YanqunXu YanfengZhang JunyiHong HanyuGao LingliWei HanruiZheng YijiaLv XingZheng Yan-BoYang JigangGong Jian-Hua