![]() The present study was initiated to pursue this question using patch-clamp techniques. Although experiments have suggested an interaction between Bcl-2 and mitochondrial channels, little is known of how this takes place. These experiments suggest that the protective effect of Bcl-2 may involve inhibition of the opening of mitochondrial channels induced by Ca 2+. Finally, Bcl-2 decreased a Ca 2+ store depletion response that opens Ca 2+ channels of the plasma membrane, the so-called capacitative calcium entry. In addition, Bcl-2 overexpression decreased the magnitude of cytoplasmic and mitochondrial Ca 2+ transients induced by inositol 1,4,5-triphosphate generating compounds. The Bcl-2 overexpression reduced the Ca 2+ levels in the endoplasmic reticulum and Golgi. More recently, experiments with Bcl-2 overexpressing cells were carried out using organelle-targeted aequorin, a Ca 2+-sensitive photoprotein. In addition, Bcl-2 antibodies stimulated the permeability transition of hepatoma mitochondria. ![]() The different properties of the two sets of mitochondria were ascribed to the increased amount of Bcl-2 in the hepatoma mitochondria estimated by Western blotting. Similar results were obtained comparing normal liver mitochondria to hepatoma mitochondria that overexpress Bcl-2. inhibition of NADH-dependent respiration. Overexpression of Bcl-2 increased the capacity of mitochondria to accumulate Ca 2+ and resist Ca 2+-induced respiratory injury, e.g. The opening of the channels may be attributed to Ca 2+ since Ca 2+ is a well-known mediator of neurotransmitter release by exocytosis. demonstrated the opening of high conductance mitochondrial channels (possibly MCC) in pre-synaptic terminals of the squid following stimulation. Ca 2+ participates in apoptosis and, in addition, has been shown to open the MCC. The effect of Ca 2+ is of particular interest. Experiments in which blockage of the permeability transition also prevented apoptosis support this model. The permeability transition is, in fact, triggered by many agents such as Ca 2+ and activated oxygen that are implicated in apoptosis. Conversely, Bcl-2 was found to inhibit the opening of the PTP. The involvement of the PTP is supported by its binding of the pro-apoptotic factor Bax. This swelling ruptures the outer membrane and spills pro-apoptotic factors into the cytoplasm. Opening of this megachannel or multiple conductance channel (MCC) (also referred to as the permeability transition pore or PTP, see ) causes swelling of the matrix space. ![]() One model for initiation of apoptosis proposes that release of the mitochondrial components of the cascade is the result of opening a megachannel in the mitochondrial inner membrane (e.g. In addition, the anti-apoptotic factor, Bcl-2, is located in mitochondria and its presence prevents the release of cytochrome c. cytochrome c, from the intermembrane space of mitochondria is involved in the commitment step of the apoptotic cascade. Release of various mitochondrial components, e.g. Lists Unordered Lists Ordered Lists Other Lists HTML Block & Inline HTML Classes HTML Id HTML Iframes HTML JavaScript HTML File Paths HTML Head HTML Layout HTML Responsive HTML Computercode HTML Semantics HTML Style Guide HTML Entities HTML Symbols HTML Emojis HTML Charset HTML URL Encode HTML vs.Mitochondria play a pivotal role in the process of apoptosis. ![]()
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