Which pathway is involved in the extrinsic pathway of apoptosis?

The extrinsic pathway of apoptosis is primarily initiated through ligand-receptor interactions. In this pathway, external signals, often in the form of death ligands such as Fas ligand (FasL) or tumor necrosis factor (TNF), bind to their specific receptors on the cell surface. This binding activates a series of signal transduction cascades that eventually lead to apoptosis.

When these ligands attach to their receptors, they trigger the recruitment of adaptor proteins and the activation of caspases, which are enzymes that execute the death program by cleaving specific cellular substrates leading to cellular disassembly and death. This is a fundamental mechanism by which the immune system eliminates unwanted or potentially harmful cells, such as infected or cancerous cells.

In contrast, the intrinsic mitochondrial pathway, which is associated with the responses to internal stressors like DNA damage or oxidative stress, is not part of the extrinsic pathway. This intrinsic pathway often involves the release of cytochrome c from mitochondria and operates through different mechanisms. Similarly, the DNA damage response and cell cycle checkpoint pathways are related to cellular repair mechanisms and the control of cell division but do not directly mediate the extrinsic apoptosis pathway. Thus, ligand-receptor interactions stand out as the critical initiating event