RISC antibody
- Known as:
- RISC (anti-)
- Catalog number:
- orb100392
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- RISC antibody
Ask about this productRelated genes to: RISC antibody
- Gene:
- SCPEP1 NIH gene
- Name:
- serine carboxypeptidase 1
- Previous symbol:
- -
- Synonyms:
- RISC
- Chromosome:
- 17q22
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-02
- Date modifiied:
- 2012-09-20
Related products to: RISC antibody
Related articles to: RISC antibody
- Crohn's disease (CD) is a chronic inflammatory condition of the gastrointestinal tract, where oxidative stress is a significant contributing factor to its pathogenesis. This study utilized multi-omics data, including RNA sequencing from the GSE216447 dataset and three genome-wide association studies (GWAS) datasets (ieu-a-10, ieu-a-11, ieu-a-13), to investigate the molecular networks related to oxidative stress in CD. Differential expression analysis was performed using DESeq2, followed by pathway enrichment analysis with clusterProfiler. Protein-protein interaction (PPI) networks were constructed using the STRING database. Mendelian Randomization (MR) analysis was conducted using TwoSampleMR and MRMix to identify causal relationships between genetic variants and CD. Quantitative real-time polymerase chain reaction (qPCR) was further applied to verify key differentially expressed genes (DEGs), including FASN, HMGCR, ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1, in intestinal mucosal samples from both inactive and active CD patients. The analysis identified 64 up-regulated and 46 down-regulated differentially expressed genes (DEGs) in response to HO intervention. Key pathways related to oxidative stress, including the p53 signalling pathway and steroid biosynthesis, were significantly enriched. Consistent with transcriptomic data, qPCR confirmed that FASN and HMGCR were significantly upregulated in inactive CD, while ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1 were markedly increased in active CD (all pā<ā0.05). The MR analysis revealed that in the dataset ieu-a-10, ABCB9 and OSGIN1 were identified as having a significant causal relationship with CD using TwoSampleMR, while only OSGIN1 was significant in MRMix. In dataset ieu-a-11, ARL4C, CD101, HMGCR, and IL24 were found to be significantly associated with CD, with overlapping findings between TwoSampleMR and MRMix. For dataset ieu-a-13, ACTA2 and CD101 were consistently identified as significant, suggesting their potential roles in CD pathogenesis. The findings highlight the crucial involvement of oxidative stress-related molecular networks in CD and underscore the utility of Mendelian Randomization in elucidating causal genetic factors. qPCR validation confirmed persistent upregulation of lipid metabolism genes in inactive CD and significant elevation of inflammation-related genes in active CD, reinforcing the link between oxidative stress and disease activity. - Source: PubMed
Yang JuanZhang LidaWang XiaqingYang Yuxiu - Adipogenesis from mouse embryonic stem cells (mESCs) offers a tractable model for dissecting early adipocyte commitment, yet the mechanisms coordinating this transition across multiple biological layers remain incompletely understood. Here we present the first simultaneous five-layer multi-omics characterization of mESC-derived adipocyte differentiation, integrating transcriptomics, proteomics, secretomics, lipidomics, and metabolomics from matched adipogenic (Pos) and non-differentiating (Neg) cell populations at day 30. Applying Multi-Omics Factor Analysis (MOFA+), we identified a dominant shared latent axis that perfectly segregated Pos from Neg cells across all five views. Layer-specific functional enrichment converged on two principal biological axes: ECM remodeling - encompassing collagens, laminins, thrombospondins, and lysyl oxidases - and lipid metabolic reprogramming, with phospholipid and glycerolipid metabolic processes dominating the lipidomics/metabolomics layer. Ensemble Machine Learning Feature Ranking (EMFR) identified a secreted factor (Scpep1; importance score 0.90) as the top-ranked discriminatory feature. Network analysis revealed indirect ECM-lipid connectivity mediated by four bridging nodes (Plod1, Thbs2, Plg, Pmp22) through a hub subnetwork of phospholipid-metabolizing enzymes. Targeted qPCR validation of six candidate regulators (Itga5, Igfbp6, Pik3cg, Lpl, Acer3, Sirt1) confirmed RNA-seq concordance. These findings establish convergent ECM remodeling and lipid metabolic reprogramming as central axes of adipocyte identity acquisition from mESCs. - Source: PubMed
Publication date: 2026/06/02
Al-Sayegh MKhalili MAlzaabi MSultana MAli LAli MEl-Hadidi M - Transcriptome-wide association study (TWAS) contributes to discovering novel susceptibility genes related to diseases. Single-cell RNA sequencing (scRNA-seq) has been extensively applied to characterize cellular heterogeneity in various biological and pathological conditions. However, few studies have integrated TWAS and scRNA-seq to decode the pathogenesis of myasthenia gravis (MG) at cellular resolution. - Source: PubMed
Publication date: 2026/05/01
Li ShuangZhang YifanHou ChenluChang Ting - Idiopathic pulmonary fibrosis (IPF) is a chronic and fatal interstitial lung disease marked by progressive extracellular matrix accumulation and irreversible lung architecture remodeling. Oxidative stress (OS) plays a crucial role in IPF pathogenesis, yet its role across distinct cellular compartments and tissue microenvironments remains incompletely characterized. - Source: PubMed
Publication date: 2025/12/08
Zhou XiangLu TongXu RanWang ChenghaoChen SimiaoChen JingChang XiaoyanLi MeifengShi JiaxinXu ChengyuZhao YupengPeng BoZhao JiayingZhang Linyou - - Source: PubMed