Autophagy is generally activated by conditions of nutrient deprivation but has also been associated with physiological as well as pathological processes such as development, differentiation, neurodegenerative diseases, stress, infection, and cancer. Atg12 is conjugated to Atg5 in a ubiquitin-like reaction that requires Atg7 and Atg10 E1 and E2-like enzymes, respectively.
The AtgAtg5 conjugate then interacts noncovalently with Atg16 to form a large complex. Autophagy and apoptosis are connected both positively and negatively, and extensive crosstalk exists between the two processes. During nutrient deficiency, autophagy functions as a pro-survival mechanism; however, excessive autophagy may lead to cell death, a process morphologically distinct from apoptosis. Additionally, Bcl-2 inhibits Beclindependent autophagy, thereby functioning both as a pro-survival and as an anti-autophagic regulator.
Mitophagy is a selective autophagic process specifically designed for the removal of damaged or unneeded mitochondria from a cell.
Upon mitochondrial damage, the protein PINK, which is continually degraded in the healthy state through the action of PARL, is stabilized and recruits the E3 ligase Parkin to initiate mitophagy. We would like to thank Prof. Request Permission for Pathway. Request Permission for Pathway.
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Save This Selection. All Rights Reserved. Pathway Description: Macroautophagy, often referred to as autophagy, is a catabolic process that results in the autophagosomic-lysosomal degradation of bulk cytoplasmic contents, abnormal protein aggregates, and excess or damaged organelles.
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