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.
The cancer cells have less amount of cholesterol and more amount of phospholipid. This structural change in the cell membranes of the cancerous cells allows a more fluid movement of the proteins. Different proteins like the MAPK or the related kinases that allows rapid cellular development and growth in the cancer cells gets easy access and movement due to the decrease amount of cholesterol and thus has an increased fluidity. Thus if somehow by using some appropriate drugs like licofelone, the cholesterol and the phsopholipid levels in the cancer cells are increased then the free fluidic movement of the cellular proteins would become difficult. No access to cell division proteins and no movement of the lipid rafts in the high hydrophobic phospholipid and dense cholesterol would inhibit the cancer cell growth and lead to apoptic cycles killing the cells.
Cancer cells typically have less cholesterol and more phospholipid in their cell membranes. This phenotype is...
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...
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.
immunology practing samples and not sure if my answers correct. 1. NK cells are effective against viral infections because many virus infected cells a. are susceptible to lysis b. are susceptible to phagocytosis c. show reduced levels of MHC class I molecules d. show reduced levels of MHC class II molecules e. none of the above 2. Arachidonic acid serves as a substrate in the lipoxygenase and cyclooxygenase pathways resulting in the production of a. histamine, leukotrienes b. leukotrienes, prostaglandins...