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.

Theoretical study shows how enzymes can achieve substrate proofreading by taking advantage of existing molecular gradients in the cell while not being endowed with structural features typically required for proofreading.

Structural biology has elucidated the mechanism of a configuration-specific enzyme that decouples D-amino acids from the translational machinery and, therefore, is involved in the enforcement of homochirality during protein synthesis.

A light-controllable ligand is used to probe where in the signaling cascade T cells discriminate self from non-self.

Direct control of ligand binding half-life with light shows that lifetime strongly affects T cell signaling.

Controlling the duration of ligand binding to the T cell receptor by light shows that T cells discriminate stimulatory from non-stimulatory ligands by measuring the dynamics of ligand binding.

Along with preventing D-amino acids from being incorporated into proteins, D-aminoacyl-tRNA deacylase clears achiral glycine that is incorrectly attached to tRNA^Ala.

KDEL receptor structures with variant HDEL and RDEL signals help decode the cell biological mechanism for the selective retrieval of escaped endoplasmic reticulum luminal proteins.

Identification of a two-tier functional redundancy to combat proteostasis imbalance induced due to tRNA expansion and oxidative stress in multicellular animals.

The ability of the T cell receptor to discriminate ligands is imperfect, allowing T cells to respond to ultra-low-affinity ligands.