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.

The asymmetric combination of saturated and polyunsaturated acyl chains in phospholipids as typically observed in synapses makes membranes prone to deformation and fission without compromising their impermeability.

Molecular pathways controlling autophagic cell death are regulated at the level of the lysosome through the activity of the pro-death Bcl-2 family member Bax/Bak.

Low-field single-sided magnetic resonance diffusion methods detect and measure permeability of sub-micron compartments which likely include cell processes, organelles, and cellular vesicles within ex vivo mouse spinal cords.

The notion that the lumen of the ATP synthase membrane rotor is the long-sought megachannel that triggers the onset of the mitochondrial permeability transition is found to be inconsistent with its actual structural and functional properties.

Bacillus subtilis can measure the activity of the enzymes that remodel the cell wall to ensure that the levels of activity are ‘just right’.

Shortage of blood-borne apolipoprotein-M–bound sphingosine-1-phosphate, which accompanies various brain disorders, causes paracellular leak and increase in transcytosis at the blood–brain barrier, which can be reversed, thus is of clinical relevance.

Ligand-induced two-fold symmetric arrangement in TRPV2 is observed in the native-like nanodisc-reconstituted condition using cryo-electron microscopy.