Functional annotation tables derived from RNA-Seq analysis of GV1001-treated experimental autoimmune encephalomyelitis mouse spinal cord

The dataset contains RNA-seq–based functional annotation tables from spinal cord tissues of GV1001-treated and vehicle-treated experimental autoimmune encephalomyelitis (EAE) mice: Table 1: Contains a full list of differentially expressed genes (DEGs) in spinal cords of GV1001-treated versus vehicle-treated EAE mice. Each gene entry includes fold change values, statistical significance metrics, and annotation fields. Table 2: Gene Ontology Biological Process (GOBP) enrichment results for the DEGs. DEGs upregulated and downregulated by GV1001 are analyzed separately. The top enriched terms indicate increased neuronal activity and decreased immune activation. Table 3: Cell-type mapping of GV1001-responsive genes. DEGs were matched with expression signatures from single-cell transcriptomic datasets to identify enriched CNS cell types (e.g., microglia, OPCs, astrocytes, neurons). Table 4: Focuses on microglial gene expression changes. Genes are ranked based on fold-change and scoring metrics derived from RNA-seq analysis. This table highlights microglial targets that may mediate therapeutic effects of GV1001. Table 5: GOBP terms enriched among GV1001-responsive microglial genes. Results show suppression of innate immune activation and enhancement of cellular differentiation, repair, and metabolic processes. Table 6: KEGG pathway enrichment for microglial genes altered by GV1001. Downregulated pathways include cytokine–cytokine receptor interaction, lysosome, and phagosome signaling; upregulated pathways include cell survival and metabolic modules.本数据集包含经GV1001处理与载体处理的实验性自身免疫性脑脊髓炎（EAE）小鼠脊髓组织的基于RNA测序（RNA-seq）的功能注释表。 表1：收录了GV1001处理组与载体处理组EAE小鼠脊髓组织中全部差异表达基因（DEGs）列表。每个基因条目包含折叠变化值、统计学显著性指标及注释字段。 表2：针对差异表达基因的基因本体生物学过程（GOBP）富集分析结果。GV1001上调与下调的差异表达基因分别进行分析，其富集度最高的条目分别对应神经元活动增强与免疫激活减弱。 表3：GV1001响应基因的细胞类型映射。将差异表达基因与单细胞转录组数据集的表达特征进行匹配，以鉴定富集的中枢神经系统（CNS）细胞类型，例如小胶质细胞、少突胶质细胞前体（OPCs）、星形胶质细胞、神经元。 表4：聚焦小胶质细胞基因表达变化。基于RNA-seq分析得到的折叠变化与评分指标对基因进行排序，该表格突出了可能介导GV1001治疗效应的小胶质细胞靶点。 表5：GV1001响应的小胶质细胞基因所富集的GOBP术语。分析结果显示先天免疫激活被抑制，而细胞分化、修复及代谢过程得到增强。 表6：GV1001调控的小胶质细胞基因的京都基因与基因组百科全书（KEGG）通路富集分析结果。下调通路包括细胞因子-细胞因子受体相互作用、溶酶体及吞噬体信号通路；上调通路包括细胞存活与代谢模块。