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The statement regarding apoptosis that accurately describes a key mechanism is that apoptosis can be promoted by the release of cytochrome c into the cytosol from mitochondria. This process is critical in the intrinsic apoptosis pathway. When a cell receives pro-apoptotic signals or experiences cellular stress, certain proteins, such as Bax and Bak, are activated and lead to permeabilization of the mitochondrial membrane. This result allows cytochrome c, a protein normally housed within the mitochondria, to be released into the cytosol.

Once in the cytosol, cytochrome c interacts with Apaf-1 and ATP, forming a complex known as the apoptosome. This complex then recruits and activates procaspase-9, which initiates the caspase cascade, ultimately leading to cellular death in a controlled manner. This mechanism is essential for the regulation of development and the elimination of damaged or unwanted cells, maintaining cellular homeostasis and preventing diseases such as cancer.

The other statements do not accurately depict the mechanisms of apoptosis. The expression of Bcl2 actually results in the promotion of cell survival, not apoptosis. The prodomain of procaspases does not contain catalytic activity; their activation upon apoptosis involves cleavage by initiator caspases.