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When mismatch repair is compromised heterozygous loss of Pol ε proofreading is sufficient to drive a subset of the observed clinical characteristics of Pol ε tumors.

Vanishing White Matter Disease mutations compromise the function of the essential translation initiation factor eIF2B by destabilizing the holoenzyme, and the small molecule ISRIB reverses their pathogenic effect by promoting complex formation.

NRF2 is the mechanism through which oxidative signals directly input into the circadian clockwork to link metabolism and timekeeping in Mus musculus.

The dramatic extension of lifespan in Sirt6-deficient mice by Trp53 haploinsufficiency suggests that SIRT6 has distinct biological function from SIRT1 in regulating p53 activity and preventing cells from senescence/apoptosis.

The range of molecular forms adopted by L1 retrotransposons reflect a tapestry of lifecycle-permissive and -restrictive host-parasite interactions occurring within cells.

ERK/MAPK activity is regulated by the cap-binding protein 4EHP, via translational control of the DUSP6 phosphatase.

Caged, photoactivatible sphingosine localized to mitochondria permits demonstration of the importance of subcellular localization on lipid metabolism and signaling.

Cryo-electron microscopy structures of human ribonucleotide reductase reveal molecular details of substrate selection and allosteric inhibition through assembly of its large subunit into a ring that excludes its small subunit.

Crk proteins are critical mediators of FGF signaling to control cell shape changes.

A single transmembrane E3 ligase complex can regulate protein ubiquitination at multiple organelles using interchangeable targeting subunits.