Depletion of cholesterol in the cell membrane using a drug (mevastatin) has been associated with
apoptosis in cancer cells.
a. What effect would cholesterol depletion have on the integrity of lipid rafts in the membrane?
b. Researchers found that FAS death receptor was activated in cholesterol depleted cancer cells.
Explain how activation of this receptor activates killer caspases.
c. When a caspase is converted from its inactive to its active form there are changes in the primary
and tertiary structure of the caspase. Explain this statement!
d. FAS death receptor is localized to lipid rafts! So what is your conclusion as to why mevastatin
initiates apoptosis in cancer cells?
a. Cholesterol is a critical structural component of lipid rafts, and depletion of cholesterol leads to disorganization of lipid raft microdomains.
b.Engagement of the death receptors with their cognate ligands such as FasL/CD95L, tumor necrosis factor-alpha (TNF-α), lymphotoxin-alpha (LT-α), TNF-like protein-1A (TL1A), and Apo2L/TNF-related apoptosis-inducing ligand (TRAIL), and their receptors promotes recruitment and activation of the apoptosis-initiating proteases, caspase-8, and caspase-10
c.
d.Mevasatatin reduces cholestderol level in body. Depletion of cholesterol leads to disorganization of lipid raft microdomains. Since FAS death receptor is localized to lipid rafts, they get exposed to their ligands like apoptosis-inducing ligand (TRAIL), and their receptors promotes recruitment and activation of the apoptosis-initiating proteases, caspase-8, and caspase-10
Apoptosis(cell death) results from a post-translational pathway driven largely by specific limited proteolysis.
Depletion of cholesterol in the cell membrane using a drug (mevastatin) has been associated with apoptosis in cancer cells. a. What effect would cholesterol depletion have on the integrity of lipid ra...
Knowing that FAS death receptor was activated in cholesterol depleted cancer cells. Explain how activation of this receptor activates killer caspases. Explain all downstream events after activation of death receptor and stopping with how activation of execution caspases occurs.
Cancer cells typically have less cholesterol and more phospholipid in their cell membranes. This phenotype is also associated with resistance to apoptosis. The FAS death receptor is localized to lipid rafts. Using this information to explain why increased phospholipid and increased cholesterol could inhibit the initiation of apoptosis. Rubric (2): Plausible link between increased change in membrane composition, effect on lipid raft formation and lack of FAS receptor activation.
Part 1: what might cause lysosomes to change their location in the cell so they could fuse with the plasma membrane. Part 2: 2-hydroxyoleic acid can increase the activity of sphingomyelin synthase causing the cells to stop dividing and initiate apoptosis! The FAS death receptor (UNIT3) is localized to lipid rafts. Explain why 2-hydroxyloleic acid treatment could cause a cancer cell to initiate apoptosis.