BIOM20001 Lecture Notes - Lecture 59: Urinary Tract Infection, Bronchitis, Necrosis
Document Summary
Balance between pro and anti-apoptotic proteins (of the bcl-2 family) that determines whether it undergoes apoptosis (don"t need to know bcl-2 etc. ) In response to cell injury these events cause change in balance - ultimately, the change in balance leads to retention (if anti-apoptotic) or release of cytochrome c from mitochondria into the cytoplasm which initiates apoptosis (if pro-apoptosis) Direct or indirect through ros if aerobic respiration goes awry. If the injury cannot be repaired the cell triggers intrinsic apoptosis . To prevent the risk of propagating a mutation that leads to neoplasia/cancer development. Accumulation of misfolded proteins (due to mutation like in familial. This accumulates which activates caspases (initiators and executioners of apoptosis). The top right animal has much marker=much caspases=much apoptosis. Not examinable (death receptor) extrinsic apoptosis pathway (signal from outside) Caused by death receptor ligand interaction (not mitochondria) Response of the host to eliminate infected cell.
