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14 Cards in this Set
- Front
- Back
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Cytotoxic Death induced by T Cells
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Defense mechanism against viruses and tumors
Responsible for rejection of transplants Secrete perforin and then is able to cleave proteins at aspartate residues |
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What is used to inhibit the Extrinsic (death receptor pathway) in Apoptosis?
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The enzyme FLIP which binds to pro-caspase 8
Both virsus and normal cells use this to protect against Fas-mediated apoptosis |
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Extrinsic (Death receptor pathway) for Apoptosis
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FasL Comes in and binds to eith TNFR1 or Fas (CD95)
FADD is then formed and binds to caspase 8 or 10 multiple times this happens until it becomes active and mediate the execution phase |
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Intrinsic (Mitchondial) Pathway for Apoptosis
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Result of increased mitchondrial permeability and the release of pro-apoptotic molecules
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Bcl-2 and Bcl-x
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Two main anti-apoptotic molecules which function to regulate apoptosis intrinsic
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What happens when the levels of Bcl-2 and Bcl-x are decreased?
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The permiability of mitochondria increases and several proteins that activate caspase leak out
Most common leak is of cytochrom c |
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Which caspases are intiators and which are executionars?
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Caspase 8 & 9 are intiator
Caspase 3 & 6 are executioners |
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p53
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Accumulates when there is DNA damage are arrests the cell cycle to allow for repair
If beyond repair then it also triggers apoptosis |
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Bax, Bak and Apaf-1
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These proteins activate caspases (intrinsic) and cause apoptosis
p53 can stimulate the production of them |
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Disorders associated with defective apoptosis
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Cancer (especially mutated p53)
and Autoimmune diseases |
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Disorders associated with overactive apoptosis
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Neurodegenerative disease
Ischemic injury (MI) Death of virus infected cells |
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What changes in drug "adaption"?
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The SER becomes hypertrophyed
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Steatosis
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Accumlation or fatty change in an organ often the liver
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Chaperones
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Aid in proper protein folding and in transport across the ER, Golgi
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