17.20 : Autophagy
Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation, hyperthermia, hypoxia, and aging. The component to be digested is sequestered, transported to lysosomes, and degraded there. The process often results in lysosomal remnants such as lipofuscin granules and residual bodies.
Studies indicate that a marked increase in autophagy maintains survival during starvation. Mammalian liver cell mitochondria are estimated to undergo autophagy every 10 minutes.
Defective autophagy, occurring during lysosomal storage diseases or certain neurodegenerative diseases, may prevent the degradation of invading microbes, unwanted or abnormal proteins resulting in infections, neurodegenerative disorders, and even cancers. Experimentally blocking autophagy in a particular portion of the brain shows an extensive loss of nerve cells, revealing the role of the process in protecting the cells.
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17.20 : Autophagy
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17.1 : Introduction to Membrane Traffic
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17.2 : COP Coated Vesicles
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17.3 : Clathrin Coated Vesicles
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17.4 : Phosphoinositides and PIPs
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17.5 : Coat Assembly and GTPases
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17.6 : Pinching-off of Coated Vesicles
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17.7 : Rab Proteins
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17.8 : Rab Cascades
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17.9 : SNAREs and Membrane Fusion
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17.10 : Vesicular Tubular Clusters
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17.11 : ER Retrieval Pathway
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17.12 : Golgi Apparatus
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17.13 : Protein Glycosylation
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17.14 : Proteoglycans
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