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Taken together, the findings of Lama et al. suggest that amicoumacin A provokes perturbation of the cell membrane and consequent energy dissipation (Lama et al. 2012).
An identical finding showed the attachment of ZnO-NPs to outer cell wall and passing in the inner wall, causing disruption of the membrane and consequent disorder and leakage [46].
The array of synthetic cells generated in this way can then be used for studies into the transport of material across a cell membrane and consequent metabolic functions, in a controlled and repeatable manner.
On the other hand, loss of Δψm could induce the opening of the permeability transition pore in the inner mitochondrial membrane and consequent rupture of the outer mitochondrial membrane, which may allow the release of proteins that reside in the intermembrane space, including cytochrome c, to activate the caspase cascade that executes the apoptotic program [51], [52].
It has been shown that dysferlin is required for the fusion of intracellular vesicles to the membrane and consequent resealing of the sarcolemma after external damage.
In TRAIL-resistant nonsmall cell lung cancer (NSCLC) cells, c-FLIP and RIP, have been shown to be essential for TRAIL-induced formation of the DISC in nonraft domains of the plasma membrane and consequent activation of NF- κβ and ERK cell survival signals.
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The major mechanism of amicoumacin A activity against pathogens involves disruption of cell membranes, and consequent cell lysis.
The major mechanism of this anti-Vibrio activity appeared to involve disruption of cell membranes, and consequent cell lysis.
Our observations of reduced cell density (Fig. 3), formation of membrane holes, disappearance of cellular contents, and formation of cell cavities (Figs. 4, 5) indicates that the major mechanism of amicoumacin A activity against pathogens involves disruption of cell membranes, and consequent cell lysis.
The intrinsic apoptotic pathway is also called the mitochondrial pathway because it is associated with the disruption of mitochondrial outer membranes and consequent release of cytochrome c.
Tubular cell toxicity due to amphotericin B depends on its binding to sterols of cell membranes and consequent alteration of membrane permeability to sodium; the increase of intracellular sodium concentration and the activation of vasoconstrictor prostaglandins lead to vasoconstriction of renal vessels.
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