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Mutant-selective AKT inhibition through lysine targeting and neo-zinc chelation
Nucleosome flipping drives kinetic proofreading and processivity by SWR1
Identification and genetic dissection of convergent persister cell states
Immune responses in checkpoint myocarditis across heart, blood and tumour
A cellular basis for mapping behavioural structure
Preferential occurrence of fast radio bursts in massive star-forming galaxies
Autonomous mobile robots for exploratory synthetic chemistry
Selective ion transport through hydrated micropores in polymer membranes
Coordinated inheritance of extrachromosomal DNAs in cancer cells
A new kind of mitochondrion
Don’t blame search engines for sending users to unreliable sites
Mechanistic understanding and efficient engineering of crystal phases in 2D materials
The antibodies don’t work! The race to rid labs of molecules that ruin experiments
Creating new materials by turning failure on its head
Author Correction: Differentiation fate of a stem-like CD4 T cell controls immunity to cancer
Amid the uncertainty, here’s what Trump’s victory might mean for U.S. science
Nine factors that could shape the research world in the next 4 years
Trump won. Is NIH in for a major shake-up?
Congress might serve as a bulwark, but some changes may be coming
When is it too hot to use a fan?
Climate chamber experiments in older people offer conflicting answers
Microglia depletion reduces human neuronal APOE4-related pathologies in a chimeric Alzheimer's disease model
Despite strong evidence supporting the important roles of both apolipoprotein E4 (APOE4) and microglia in Alzheimer's disease (AD) pathogenesis, the effects of microglia on neuronal APOE4-related AD pathogenesis remain elusive. To examine such effects, we utilized microglial depletion in a chimeric model with induced pluripotent stem cell (iPSC)-derived human neurons in mouse hippocampus. Specifically, we transplanted homozygous APOE4, isogenic APOE3, and APOE-knockout (APOE-KO) iPSC-derived...
Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging
To systematically characterize the loss of tissue integrity and organ dysfunction resulting from aging, we produced an in-depth spatial transcriptomic profile of nine tissues in male mice during aging. We showed that senescence-sensitive spots (SSSs) colocalized with elevated entropy in organizational structure and that the aggregation of immunoglobulin-expressing cells is a characteristic feature of the microenvironment surrounding SSSs. Immunoglobulin G (IgG) accumulated across the aged...