Entry processes into cytosol

However, the current view of the regulation of calcium ion entry into the cytoplasm by PLC-linked stimuli holds that activation occurs not as a direct result of the action of IP3 on the plasma membrane but indirectly, as a result of depletion of calcium ions from an intracellular store by IP3 [14]. In the context of this capacitative model , the actions of intracellularly applied IP3 and heparin reflect the effects of these maneuvers on intracellular release process from ER into cytosol, rather than via the plasma membrane. The reported actions of I(1,3,4,5)P4, if in fact they do represent physiological control mechanisms, may reflect an ability of I(1,3,4,5)P4 to augment the calcium-releasing ability of IP3, rather than a distinct and... 

At this point, the acyl-CoA is still in the cytosol of the muscle cell. Entry of the acyl-CoA into the mitochondrial matrix requires two translocase enzymes, carnitine acyl transferase I and carnitine acyl transferase II (CAT I and CAT II), and a carrier molecule called carnitine the carnitine shuttles between the two membranes. The process of transporting fatty acyl-CoA into mitochondria is shown in Figure 7.15. 

Figure 20.19 Summary of transcription, RNA splicing entry of mRNA into the cytosol and polypeptide formation. The difference in shading is to indicate the change from DNA to RNA. Splicing is just one of the four processes involved in the processing of the primary RNA transcript (Figure 20.20).

Figure 20.34 A simple representation of the processes of necrosis and apoptosis leading to the death of cells. Necrosis is initiated by a decrease In the ATP/ADP concentration ratio, which slows ion pumps, which leads to cation imbalance (e.g. ca ion entry into the cytosol) and hence intracellular damage, entry of water and lysis which can lead to local inflammation. Apoptosis is initiated by specific extracellular or intracellular factors, which lead to cell shrinkage and disruption into apoptotic bodies which are removed by phagocytes.

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