The Intrinsic Pathway of Apoptosis

摘要: Virtually all anticancer drugs induce apoptosis in susceptible cell types. This biochemically distinct form of death reflects, large part, activation caspases, a family intracellular cysteine proteases. At least two separable processes, one starting with ligation specific surface receptors (so-called receptors) and the other involving release cytochrome c from mitochondria, result transduction various signals into caspase activity. The mitochondrial or intrinsic pathway appears to play predominant role apoptotic response drugs. Bcl-2 members regulate this by modulating key proapoptotic polypeptides, including second activator caspases (Smac)/direct inhibitor (IAP)-binding protein low pI (DIABLO), mitochondria. Several that facilitate permeabilization are transcriptional targets p53 tumor suppressor gene, providing partial explanation for ability DNA-damaging agents apoptosis. Other released cytoskeletal sites upon treatment paclitaxel loss adherence. antiapoptotic XIAP (X chromosome-linked IAP) binds procaspase 9 prevents its activation. gene encoding is activated nuclear factor-κB, contributing effects transcription factor. In chapter, components reviewed, alterations cancers described, evidence some these same might contribute drug resistance under certain circumstances discussed.