Genetic and molecular analyses identify and characterize an evolutionary battle over lysis timing wherein a bacteriophage delays lysis through lysis inhibition while a defensive phage satellite accelerates lysis.
A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.
In behaving mice, inhibition from molecular layer interneurons attenuates excitation of Purkinje cells by parallel fibers and suppresses their ability to enhance climbing fiber-triggered dendritic Ca2+ responses.
Sst+ interneurons drive feedforward inhibition in the basolateral amygdala, and thus provide a framework for why interneuron subtypes may mediate different archetypal circuit motifs across different brain regions.
Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.