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.

Recurrent neuronal networks learn to predict movement in a self-supervised way using biologically plausible learning rules.

The different polymerases at eukaryotic replication forks achieve their asymmetric placement on the leading and lagging strands through exclusion processes that prevent their function on the 'wrong' strand.

DnaB Helicase is the only stable component of the bacterial replisome as the replicative DNA polymerase frequently exchanges in both leading and lagging strands.

A novel pair of isobaric crosslinking reagents is described, which allow relative quantification of crosslinker-modified peptides during mass spectrometry analysis for comparative structural studies of proteins and protein complexes.

In mature neurons, TSPAN5 assembles into a complex with AP4 and Stargazin to promote the exocytosis of AMPA receptors.

A multi-step process of helicase activation sensitizes replication initiation to the extent of replicative helicase phosphorylation.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

The TPL corepressor binds to the core mediator complex through MED21 to inhibit transcription while simultaneously priming repressed genes for rapid reactivation.