Aggregate-prone proteins (e.g. those with expanded stretches of glutamine residues in diseases like Huntington’s disease) will cause
neuronal cell death
Autophagy degrades _______. No toxic stimulus, no _______.
Many proteins - e.g. Bcl-2 - that regulate apoptosis/ cell death, also control
autophagy–remember, this could create problems in interpreting results of therapeutic interventions designed to target these proteins.
_______ can cleave essential autophagy regulators, _______ them and therefore _______ the process of autophagy.
_______(best studied)- form a double membrane vesicle that captures cytosolic components/organelles. Then fuse with lysosome where hydrolases degrade contents of autophagosome.
Macroautophagy
Macroautophagy (best studied)- form a _______ that captures cytosolic components/organelles. Then fuse with _______where hydrolases degrade contents of _______.
Macroautophagy (best studied)- form a double membrane vesicle that captures _______. Then fuse with lysosome where _______ degrade contents of autophagosome.
- hydrolases
_______–recognition of specific proteins that contain a specific recognition sequence (based on amino acid sequence KFERQ). Direct binding and delivery to lysosome.
Chaperone-mediated
Chaperone-mediated–recognition of specific proteins that contain a _______. _______binding and delivery to lysosome.
Chaperone-mediated–recognition of specific proteins that contain a specific recognition sequence (based on amino acid sequence KFERQ). Direct binding and delivery to _______.
lysosome
macroautophagy 1: Activate a _______ that allows _______ that will eventually form an _______.
-PI3K complex
nucleation of a membrane
-autophagosome
macrophagy 2: Regulation of _______
-protein conjugation events to extend membrane.
macrophagy 3: Randomly capture, or specifically deliver cargo to _______, then _______ to _______.
macrophagy 4: Fuse with _______. Recycle _______ and _______