ANAT 365 Lecture Notes - Lecture 14: Rheb, Genome Instability, Autophagy
19 Jul 2016
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Document Summary
Macroautophagy: large membrane structures wrap around proteins aggregates/mitochondria/organelles, etc. Microautophagy: small cell constituents invaginate directly into late endosome intraluminal vesicles. Chaperone-mediated autophagy: take unfolded proteins from cytosol translocate to lumen of lysosomes. Pathways to lysosome don"t have to come from cell surface can also come from other areas of cell. If no autophagy: accumulation of damage & oxidative stress genome instability. Autophagy prevents genome instability, oxidative stress, and inflammation. Autophagy activated in starvation not enough nutrients. Stop energy storage & utilization (stop synthesis), promote nutrient uptake & recycling. Gap is tsc: causes rheb hydrolyze gtp gdp inactive rheb inactive mtor. Low energy: ampk phosphorylates tsc (gap) active shut down torc. Growth factors inactivate tsc active rheb & tor. Prak phosphorylates gdp-rheb to stabilize inactive inactive torc. Ragulator recruits ragd & ragb to lysosome, ragulator acts as gef. Add aa activate rheb recruits torc to lysosome membrane. Torc phosphorylates atg13 & ulk1/2 inactivates initiators of autophagy (low nutrients)
