Key Highlights
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Cancers evade RAS-targeting molecular glues through distinct alterations that converge on disrupting synthetic complex formation. This work exposes strategies for improved drug design and rational combination therapy to overcome resistance.
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Cytosolic DNA, derived from cellular damage or microbial infection, interacts with key components of the RNA polymerase I transcription machinery and retains them in the cytoplasm. This inhibits rDNA transcription, suppresses protein synthesis, and curtails cell proliferation, revealing a novel role for cytosolic DNA beyond immune activation.
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An author correction was published for a study linking an emerging human eye disease to aquatic virus zoonotic infection. The original work was published in Nature Microbiology.
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