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Showing posts from July, 2015

Autophagy and Apoptosis

The p53, a protein that assists in the cell cycle arrest, takes the cell out of the cycle for autophagy and repairs, or self-destruction by apoptosis. The eventual viable cell then re-enters the cycle. The p53 gene is a potent anti-oncogene. When mutated, the cell will continue to carry out cell-cycling, unabated, and replication will continue--including of the telomere repeats-- as normal. There are isoforms of p53 involved, which sense the need for either apoptosis, or autophagy and repairs. Autophagy is anti-inflammatory as the cell is kept viable, shows no signs of distress(damage), safe, perhaps, for some cell shrinking(due to self-cannibalization of up to 50%)-- thus, there is no need to call for inflammatory cells. Equally, autophagy disposes of the inflammasome. Conversely, inflammation prevents autophagy, hence the need to reduce inflammation to promote the more useful and desirable phagocytosis, since autophagy disposes of intracellular pathogens and debris. Some intra...