Human forebrain organoids reveal that amyloid-driven microglia recruit killer T cells via CCL5, forming a self-amplifying neuroinflammatory loop targetable by CCR5 or CXCR3 blockade.
In mammalian neocortex, opposing Krüppel-like factor (KLF) transcription factors first activate and then repress a genetic program related to axon outgrowth, potentially contributing to loss of cortical axon outgrowth in the adult.
Syntaxin11 directly controls a novel step in the activation of calcium channels, which helps activate genes and kill infected cells by a process distinct from moving cargo inside cells.
The activity of Dcp-1, one of Drosophila executioner caspases, is selectively regulated by the autophagy–Bruce axis, which enables distinct non–lethal functions for promoting tissue growth independent of cell death.