Apoptosis regulatory pathways

Apoptosis regulatory pathways" is not a specific molecular target, but rather a collective term describing interconnected signaling networks that control programmed cell death (apoptosis) in multicellular organisms[4][7][8]. These pathways regulate cellular fate through two main mechanisms: the **intrinsic (mitochondrial)** and **extrinsic (death receptor-mediated)** apoptotic pathways. Key molecular players include death receptors (such as Fas, TNFR1, DR4/5), adapter proteins (FADD, TRADD), caspases (initiators: caspase-2, -8, -9, -10, -11, -12; effectors: caspase-3, -6, -7), Bcl-2 protein family (anti-apoptotic: Bcl-2, Bcl-xL, Mcl-1; pro-apoptotic: Bax, Bak, Bid, Bim), mitochondrial factors (cytochrome c, Smac/Diablo), and various kinases and transcription factors (MAPK pathway, p53, FoxO)[1][2][6][7][9][10]. Dysregulation of these pathways underlies a wide range of human diseases, including cancer, neurodegeneration, and certain immune disorders. Importantly, drugs often target specific components of these pathways (such as Bcl-2 inhibitors or death receptor agonists) for therapeutic benefit in cancer and other diseases, but "apoptosis regulatory pathways" itself is not a single druggable protein, making it an improper entry for a canonical drug target database[3][5][9].

Other names

Apoptosis pathwaysCell death regulatory pathwaysProgrammed cell death pathways

Activation or inhibition of death receptors (Fas, TNFR1, DR4, DR5); Activation or inhibition of Bcl-2 family proteins (pro-apoptotic or anti-apoptotic modulation); Caspase activation or inhibition; Induction of DNA damage-mediated apoptosis; Inhibition of survival pathways (e.g., AKT, MEK); SMAC mimetic action antagonizing inhibitor of apoptosis proteins (IAP); Modulation of p53 pathway activity