Some of the mutations that occur during influenza evolution can only be tolerated in conjunction with other mutations that increase the stability of a viral protein.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

A compound that prevents stressors such as UV light and viral infection from downregulating protein synthesis inside cells improves memory performance in mice.

The transport of proteins along flagellar microtubules generates the force that enables flagella to propel cells across surfaces.

A modified form of Green Fluorescent Protein integrated into an ammonium transporter provides a sensor that can be used to monitor transport activity in vivo.

Quantitative observations of single-molecule binding between antigen and T cell receptor (TCR) in living primary T cells reveals unbinding kinetics, stoichiometry and signaling molecule recruitment, providing insights into the mechanisms of antigen recognition by the immune system.

α-SNAP mediated rearrangement of Stim1 and Orai1 molecules within CRAC channel clusters is required for store-operated calcium entry.

A key activator of Ras signaling adopts an autoinhibited, dimeric conformation that is activated by membrane and calcium binding.

The recycling of transmitter vesicles at synapses shows calcium-dependent regulation that depends on the phosphorylation status of an enzyme called dynamin.

Cells repair damage to their outer membranes not by patching them as previously thought, but by using proteins called caveolins to remove the damaged regions by endocytosis.