GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320428/suppl/filelist.txtftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320428/suppl/GSE320428_RAW.tarftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320428/primary200OKTranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE320428GEOGSEfalseGene expression profiling of vulnerable spinal motor neurons in the SMNΔ7 mouse model of SMA upon modulation of p53 signalingSelective motor neuron degeneration in spinal muscular atrophy (SMA) is driven by converging mechanisms that promote stabilization and phosphorylation of p53 in vulnerable motor neurons. However, the downstream transcriptional programs that execute motor neuron death remain incompletely defined.To characterize p53-associated transcriptional changes in vulnerable motor neurons, we performed RNA sequencing of cholera toxin subunit B (CTB)-labeled lumbar (L1–L3) motor neurons isolated by laser-capture microdissection from postnatal day 6 SMNΔ7 (SMNΔ7;SMN2;Smn−/−) SMA mice and wild-type littermate controls. Disease-associated gene expression changes were defined by comparison of SMA and wild-type motor neurons. To assess pathway-specific contributions, untreated SMA mice were compared to SMA mice treated with Pifithrin-α (inhibitor of p53 transcriptional activity), MW150 (p38 MAPK inhibitor that prevents p53 phosphorylation), or SMN-C3 (SMN splicing modifier). Differential gene expression analysis was performed using kallisto-based transcript quantification and DESeq2.2026/08/12GSE320428GSM9543184GSM9543173GSM9543183GSM9543172GSM9543175GSM9543186GSM9543185GSM9543174GSM9543177GSM9543176GSM9543179GSM9543178GSM9543180GSM9543182GSM954318124247320428Mus musculus[42395465]