Core of basic research: Focuses on the "death signal-signal transduction-apoptosis execution" molecular mechanism of apoptosis (programmed cell death), critical for maintaining cellular homeostasis and eliminating abnormal cells. Apoptosis initiation involves extrinsic (death receptor pathway) and intrinsic (mitochondrial pathway) pathways: The extrinsic pathway is triggered by death receptors (Fas, TNFR1) binding ligands (FasL, TNF-α), activating caspase-8 and cascading downstream effector caspases (caspase-3/6/7); the intrinsic pathway is induced by cellular stress (DNA damage, nutrient deficiency), increasing mitochondrial membrane permeability and releasing Cytochrome c, which binds Apaf-1 to form apoptosomes, activating caspase-9 and effector caspases. Ultimately, effector caspases degrade key proteins such as cytoskeleton and DNA repair factors, leading to orderly cell death. Research focuses include the specific recognition of apoptotic signals, regulation of mitochondrial membrane permeability, cascaded activation of caspases, the regulatory role of Inhibitors of Apoptosis Proteins (IAPs), and the association of pathway abnormalities with tumors (apoptosis inhibition) and autoimmune diseases (excessive apoptosis).
Core key proteins: Death receptors (Fas/CD95, TNFR1, DR4/DR5), death ligands (FasL, TNF-α, TRAIL), caspase family (initiators: caspase-8/9; effectors: caspase-3/6/7), Cytochrome c, Apaf-1 (Apoptotic Protease Activating Factor 1), Bcl-2 family (anti-apoptotic: Bcl-2, Bcl-XL; pro-apoptotic: Bax, Bak, Bid), IAP family (cIAP1/2, XIAP), PARP (Poly(ADP-ribose) Polymerase, apoptotic substrate), p53 (DNA damage response, regulating intrinsic apoptosis).