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A pore-forming antiphage defence is activated by oligomeric phage proteins
Signatures of fractional charges via anyon–trions in twisted MoTe<sub>2</sub>
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...