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.
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.
Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.