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Daily briefing: Could microbe-friendly buildings help us be healthier?
Cerebrospinal fluid proteomic signatures in cognitively normal individuals identify distinct clusters linked to neurodegeneration
AI bots wrote and reviewed all papers at this conference
Carbon credits are failing to help with climate change — here’s why
Inside our university’s mission to pivot to research
The race to uncover snow’s many mysteries before it disappears forever
The probiotic home: where microbes are welcome guests
The spectre of malnutrition is back and must be tackled — fast
Faulty mitochondria cause deadly diseases: fixing them is about to get a lot easier
Longer grant cycles would boost research in Africa
AI’s therapeutic potential goes beyond emotional connection
Japan declares a flu epidemic — what this means for other nations
Do rats double-dip food with their tails?
Brazil’s COP30 legacy should be to protect more of its forests
Red lines for religious AI
Gigantic black holes did not have starring role in early cosmic transition
Whiplash at CDC as hundreds of employees are terminated, then reinstated
Agency’s prestigious training programs among those spared, while other key offices are scrapped
Men's brains shrink faster than women's: what that means for Alzheimer's
No abstract
MAPL regulates gasdermin-mediated release of mtDNA from lysosomes to drive pyroptotic cell death
Mitochondrial control of cell death is of central importance to disease mechanisms from cancer to neurodegeneration. Mitochondrial anchored protein ligase (MAPL) is an outer mitochondrial membrane small ubiquitin-like modifier ligase that is a key determinant of cell survival, yet how MAPL controls the fate of this process remains unclear. Combining genome-wide functional genetic screening and cell biological approaches, we found that MAPL induces pyroptosis through an inflammatory pathway...
The interactome era: Integrating RNA-seq, proteomics, and network biology to decode cellular senescence
Cellular senescence is a dynamic state in which cells permanently withdraw from the cell cycle while continuing to reshape their internal and external environment. It is characterized by persistent DNA damage responses, chromatin reorganization, and the secretion of a complex mixture of cytokines and proteases collectively known as the senescence-associated secretory phenotype (SASP). Transcriptomic and proteomic studies have defined key markers, including CDKN2A, CDKN1A, TP53, and SASP factors,...