Neurons in the hippocampus modulate the rates at which they fire, and the locations in which they fire, so as to encode the information that is central to forming memories about personal experiences.

Long-lived intermediate states formed by glycoprotein catalysts are an essential part of the process used by influenza virus particles to infect cells.

By using different groups of cells to represent distinct environments and events, the dentate gyrus of the hippocampus helps to keep memories of similar events separate.

In a mouse model of neurodegeneration, hippocampal firing sequences that normally encode spatial memories become disengaged from external space.

Synergistic interactions with PI(4,5)P2 and activated Rho1, which are enriched at the apical membrane of tubular organs, facilitate tight apical targeting of the formin Diaphanous.

Cryo-electron tomography reveals how a chaperone protein called TRiC reduces the ability of pathogenic mutant huntingtin proteins to form aggregates.

Utilizing a conserved mechanism, a ribosome can initiate translation from a site within the insulin receptor mRNA to maintain protein synthesis even when standard mechanisms of initiating translation have been inhibited by stress.

Structural studies reveal the mechanism by which a HECT E3 ubiquitin ligase carries out E2-to-E3-to-substrate ubiquitin transfer and prioritizes target lysines for ubiquitination.

Structural analyses of the centriole proteins CPAP and STIL identify domains that are critical for centriole formation and provide a structural explanation for a mutation that causes human microcephaly.