The binding of death ligands to their receptors initiates the formation of the death-inducing signaling complex (DISC). This complex activates caspases, which are proteases that cleave specific cellular substrates, leading to the morphological and biochemical changes characteristic of apoptosis. For example, the interaction between FasL and its receptor Fas leads to the activation of caspase-8, which in turn activates downstream effector caspases like caspase-3.
