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17 Cards in this Set
- Front
- Back
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Describe necrosis.
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1. Passive
2. Rupture of the plasma memebrane is the main distinction of necrotic cell death |
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What happens during apoptosis?
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1. Cleavage of DNA into 200bp fragments
2. Cytoplasmic shrinkage and nuclear condensation 3. Cleavage of essential proteins via caspases |
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What happens to dead cells in apoptosis?
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They are packaged into apoptotic bodies and phagocytosed
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Is there inflammation around an apoptotic body?
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No
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Is apoptosis passive?
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No it is ATP dependent
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Describe extrinsic mediated apoptosis.
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1. Ligand binds to FAS receptor
2. Trimerization of FAS receptor 3. Recruitment of FAD internally 4. Recruitment of caspase 8 5. Caspace 8 recruits and activates caspase 3 6. Caspace 3 induces cleavage associated with apoptosis |
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Describe intrinsically mediated apoptosis.
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1. Some sort of stress causes the ratio of Bax (pro-apop) to Bcl-2 (anti) to shift in favor of BAX
2. This causes the releasal of Cytochrome C from the mitochondria 3. Cytochrom C, Caspase 9, Apaf1 and dATP form an apoptosome 4. The apoptosome activates caspase 3 5. Caspase 3 does the rest |
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What are the two ways that the intrinsic and extrinsic pathways of apoptosis can converge?
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1. They can converge at the level of caspase 3.
2. They can converge because caspase 8 can cause make tBid from Bid. This interacts with BAX to start the intrinsic pathways to start. |
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What accumulates in autophagic cell death?
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Autophagic vacuoles
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What causes the accumulation of autophagic vacuoles?
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Specific inhibition or activation of autophagy
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What does specific inhibition of autophagy cause?
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Prevents the recycling of components back to the mitochondria for normal function
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With autophagy, what happens to the number of mitochondria present?
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Decreases
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Does autophagy have a potential role in neurodegenerative disease?
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Yes
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What does AB come from?
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Amyloid precurson protein (APP)
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What forms plaques in AD?
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AB
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What eventually leads to cell death in AD?
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The accumulation of AB plaques (from APP).
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What are the three challenges of studying cell death in AD?
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1. Correlating in vitro/animal models with human AD
2. Chronic onset and progression 3. The amount of cell death at any one time is minimal |
