Sites at which mitochondria contact the endoplasmic reticulum co-localize the replication of mitochondria and their DNA to help ensure that DNA is distributed appropriately between the newly formed organelles in cells.

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.

Genetic and electrophysiological experiments reveal that a gene called MCU encodes the ion channel pore that allows calcium ions to cross the inner mitochondrial membrane.

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 proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.

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.