Apoptosis Flashcards From Discussion

Flashcards covering apoptosis, caspase cascade, and related pathways.

Caspases

Cleaves after Aspartate Amino Acids, zymogens with low activity that become highly active upon activation.

TNF Signaling

Signaling pathway initiated by TNF ligand binding to TNFR.

FAS Signaling

Signaling pathway initiated by FAS ligand binding to FASR, usually expressed by cytotoxic immune cells.

Extrinsic Death Receptor Pathway

Trimerization of receptors exposes death domains on cytoplasmic tails (TRADD/FADD). Death effector domains bind to procaspase 8, leading to caspase 8 activation and apoptosis.

C-FLIP

Binds to death effector domains, inhibiting procaspase 8 activation, and is often upregulated in cancer.

Intrinsic Apoptotic Regulators

Proteins that control mitochondrial permeability and are triggered by intracellular signals (DNA or oxidative damage).

Bcl-2, Bcl-xL, Mcl-1

Anti-apoptotic proteins that sequester Bak and Bax, inhibiting cytochrome C release.

Bak, Bax, Bid, Bad, Bim

Pro-apoptotic proteins that promote mitochondrial outer membrane permeabilization (MOMP) and cytochrome C release.

Apoptosome

Complex formed by cytochrome C, Apaf-1, and procaspase-9, leading to caspase-9 activation and apoptosis.

IAPs

Inhibitors of apoptosis that inhibit procaspase self-cleavage into active caspases.

Smac/Diablo

Inhibits IAPs, increasing apoptosis; acts as a tumor suppressor.

P53-death mediation

Increases pro-apoptotic signals (BAX, BAK, BID) and inhibits pro-survival pathways (PI3K-AKT-mTOR).

Transcription Independent P53 mediated death

Binds BCL2 & BCL-XL, activates Bax, and activates PUMA, promoting mitochondrial membrane insertion.

SAHA

HDAC inhibitor that epigenetically turns on Bid; used in Non-Hodgkin’s Lymphoma.

Venetoclax

Mimics BH3 domain, releasing BIM and allowing Bax to dimerize, triggering apoptosis by binding to MCL-1.