Cell Death Flashcards
Caspase 3
Activates xkr8 flipase which flips phosphotadyl serine to the outer membrane
Cleaves ipla2 which cleave phosphotadyl choline to soluble Lysol form on the outer membrane
Caspar 9 activation
Apaf1 binds cytochrome c
ATP hydrolysis causes apaf1 to oligomerise into the apoptasome exposing the card domains which bind capase 9 causing it to dimerise before it cleaves itself from the apoptasome
Bcl2
Bax bak bok
Bh3
Prevent apoptosis
Release cytochrome c from the mitochondria by puncturing holes in it
Regulates the other two groups
EGFR
Turns on the kinase signalling pathway however when phosphorylated it can cause cell death
ABT 263 drug
Induce apoptosis
Caspase 8
Activated by cell surface receptor
Tumour necrosis factor
Trimeric
CD95
Activated by cytotoxic T cells
Which cause it to oligomerise causing death domain to bind to the fadd domain allowing ded domain to cause dimerisation of caspase 8 forming the disc complex
Cd95 defects
ALPs
Mutated cd95 so the lymphocytes accumulate in the nodes causing an autoimmune lymphoid tumour
Trail receptors
Dr4,5
Not widespread
Increased expression in response to anti cancer drugs
Chemo may sensitise cancer cells to trail allowing apoptosis
Bid
Caspase 8 cleaves bid Causes mitochondrial permeabilisation allowing cyto c to inhibit the caspase 8 inhibitors such as XIAP
Pamps
Bacterial cell wall components
Microbial dna
Damps
ATP heatshock protein Uric acid
NLR
Detects pamps and damps causing oligomerisation exposing the card domains for Caspase 1 to dimerise on before it cleaves itself off and activates the inflammatory response
Autophagy activation
Lack of nutrients causes akt to be inactive and ampk to be active which inactivates mtor activating atg13 complex leading to cell auto phage
Milo phage
Auto phage of mitochondria
