Jiaying Qiu

Abstract Background Voltage-gated sodium channels (VGSCs) are fundamental to electrical signalling in excitable cells, and their dysfunction underlies a wide range of channelopathies. While the existence of nine distinct α-subunit genes contributes to VGSC diversity, alternative splicing serves as a significant post-transcriptional mechanism that profoundly expands their proteomic and functional repertoire. Dysregulation of this splicing process is increasingly linked to disease pathogenesis.

Abstract RIPK3 is a key regulator of necroptosis, but the specific roles of its kinase-dependent and -independent functions in disease pathogenesis remain poorly understood. Here, we generated and characterized RIPK3 D143N kinase-dead knock-in mice, a novel kinase-inactive model that selectively disrupts RIPK3 kinase activity without inducing spontaneous apoptosis.

Identify cell subtypes and their DEGs We next subdivided each cell type into subtypes. Astrocytes were divided into five clusters after dimensionality reduction (Fig 4A). AS-2 had progenitor cell characteristics because its markers included cell cycle–related genes like Cdca8 and Stmn1 and were significantly enriched in the cell cycle pathway (S4A and S4B Fig). AS-1 and AS-4 were defined as mature astrocytes because their marker genes were mostly found in the ribosome.