Sentence examples for membrane permeabilization resulting from inspiring English sources

BAX/BAK oligomerization causes mitochondrial outer membrane permeabilization, resulting in cytochrome c release and apoptosis.

Previous studies have reported that increase in Bax/Bcl-2 ratio can cause mitochondrial membrane permeabilization, resulting in the release of cytochrome c and induction of apoptosis [ 59].

Mitochondria of cancer cells display higher ΔΨm[ 21] and chemotherapeutic agents induce mitochondrial membrane permeabilization resulting in the collapse of ΔΨm[ 22].

This initiates the effector phase of cell death by causing mitochondrial outer-membrane permeabilization, resulting in the release of apoptogenic factors (e.g., cytochrome- c and SMAC/DIABLO) that activate the caspase cascade to mediate cellular demolition.

Once triggered, lysosomal membrane permeabilization results in the release of cathepsins and other lysosomal hydrolases to the cytosol, where they can trigger the mitochondrial outer membrane permeabilization followed by caspase-mediated apoptosis [7], [8] or mediate caspase-independent programmed cell death [9].

In healthy cells a vesicular distribution of LY is observed, whereas lysosome membrane permeabilization results in a cytosolic release of LY and a diffused cytoplasmic fluorescence.

Mitochondrial outer membrane permeabilization results in the release of pro-apoptotic factors such as cytochrome c from the mitochondria into the cytosol leading to apoptosome formation, caspase activation and DNA fragmentation.

Mitochondrial outer membrane permeabilization results in the release of cytochrome C from the intermembrane space into the cytosol, triggering the assembly of the caspase-activating complex that mediates autocleavage and activation of caspase 9 [ 32].

In the execution or post-mitochondrial phase, mitochondrial membrane permeabilization results in the breakdown of the mitochondrial transmembrane potential, respiratory chain uncoupling, ATP depletion, generation of reactive oxygen species, the release of pro-apoptotic proteins into the cytosol and finally cell death.

In further studies, CQ and HCQ are shown to function as lysosomotropic agents to promote lysosomal membrane permeabilization (LMP), resulting in signs of apoptosis.

After a death signal, Bax activation, mediated by truncated Bcl-2 homology 3 (BH3 -only protein as BH3 -onlyacting domain death agonist (Bid), leads to oligomerization and insertion to the liproteinaser of the mitochondrial outer membrane, thereby initiating a channel-like structure that causes mitochondrial outer membrane permeabilization (MOMP), resulting in cytochrome c release.