Further evidence in support of a new amyloid-independent hypothesis for the pathogenesis of Alzheimer's disease is provided, with an expanded set of Alzheimer-causing mutations in the protease that produces amyloid.
NPRL2 gene therapy induces robust antitumor immunity and overcome anti-PD1 resistance through augmenting antigen-presentation and cytotoxic T cells activation in KRAS/STK11 mutant NSCLC in humanized mouse model.
Oversized mammalian cells reduce their growth efficiency by activating global protein degradation, which functions in parallel with the cell size checkpoints, to promote cell size homeostasis.
