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Onko (Fach) / 6. Villunger (Lektion)
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- How can caspases be activated? -Caspase-activation can occur, e.g., after loss of mitochondrial integrity - Caspase activation can occur, e.g., in response to receptor/ligand interaction - Caspase activation can be, e.g., cell-cell contact mediated
- Which members of the Bcl2 family execute MOMP? Bax and Bak -> forms MOMP BH3-only proteins bind Bcl-2 homologues to promote MOMP (activates BAX and BAK)
- What is the major driver of regulated necrosis? DRs can signal necrosis (necroptosis) via RIPK1/RIPK3 kinase activity PARP?! - consumes NADH needed by the cell → necrosis
- Name possible outcomes of TNF-Receptor ligation survival, apoptosis, necroptosis; release/production of cytokines, mediation of inflammatory response and immune responses
- Which cell death signaling molecules/pathways are currently developed/targeted for anti-cancer therapy? Most Anticancer Therapies Depend on BH3-only proteins (• IR & DNA-damaging drugs -> Puma, Noxa • RTK inhibitors -> Bim, Bmf, Bad • HDACi -> Noxa, Bmf • Proteasome blocker -> Noxa, Bim • mAbs -> ADCC, loss of Bcl2/Mcl1 expression) Overcoming conventional drug-resistance by mimicing BH3-only protein function Exploiting DR signaling for anti-cancer therapy
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