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Bacterial immune activation via supramolecular assembly with phage triggers
Discovery Learning predicts battery cycle life from minimal experiments
Synthesizing scientific literature with retrieval-augmented language models
Large-scale analogue quantum simulation using atom dot arrays
Atmospheric H<sub>2</sub> variability over the past 1,100 years
PtdIns(3,5)P<sub>2</sub> is an endogenous ligand of STING in innate immune signalling
Biofluid biomarkers in Alzheimer’s disease and other neurodegenerative dementias
Regulatory grammar in human promoters uncovered by MPRA-based deep learning
Atlas-guided discovery of transcription factors for T cell programming
A universal concept for melting in mantle upwellings
These mysterious ridges could help skin regenerate
Author Correction: Cotranslational assembly of protein complexes in eukaryotes revealed by ribosome profiling
Exposure to low-credibility online health content is limited and is concentrated among older adults
The age gap of health misinformation
Quantum computers will finally be useful: what’s behind the revolution
AI research deluge: why one conference is asking authors to rank their own papers
Space dust reveals rapid evolution after dino-killing asteroid
New data detail how tiny forms of life rebounded much more quickly than previously believed
Repression of RIPK1 kinase by INPP5D inhibits expression of diverse proinflammatory mediators and late-onset Alzheimer's disease risk factors
Genome-wide association studies strongly implicate neuroinflammation in late-onset Alzheimer's disease (LOAD). Genetic risk loci for LOAD are enriched for genes expressed in microglia, but the relationship among microglial LOAD risk genes has been unclear. We found that the N-terminal SH2 domain of INPP5D, an important LOAD risk gene, directly interacted with the cell death regulator RIPK1 at p-Y383 to suppress RIPK1 kinase activation. Microglial INPP5D deficiency cell-autonomously promoted...
Gut microbiota-dependent 24-hydroxycholesterol metabolism contributes to capsaicin-induced amelioration of Alzheimer's disease-like pathology in mice
Dietary capsaicin intake appears to affect the pathogenesis of Alzheimer's disease (AD), while the underlying mechanisms remain unclear. Here, we found in human cohorts that moderate-to-high level of dietary capsaicin intake was associated with improved cognitive performance. Similarly, long-term oral capsaicin administration in male 5×FAD mice ameliorated AD-like pathologies and reshaped gut microbial composition. Gut microbiota transfer from capsaicin-treated mice produced similar effects of...
MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration
Microglial phagocytosis exerts essential roles in neurodegeneration, but how phagocytic processes may reciprocally regulate microglia remains incompletely understood. Here, we report that microglial response in the mouse model of pathological axonal degeneration depends on the phagocytic receptor MerTK. The MerTK-triggered downstream phospholipase C signal is sufficient to induce the up-regulation of PU.1 and IRF8, the two central transcription factors governing microglial functions. Chromatin...