Question

Which of the following would block release of cytochrome c from mitochondria?

I. the Bcl2 protein
II. Survival Factors
III. Fas ligand

Answer 1

The Bcl2 protein and Survival Factors can block the release of cytochrome c from mitochondria and thus prevent apoptosis. The Fas ligand, on the other hand, promotes apoptosis and would not block cytochrome c release.

Step-by-step explanation:

The release of cytochrome c from mitochondria is a crucial step in the process of apoptosis. There are several factors that can block this release and prevent apoptosis. Specifically, the Bcl2 protein is known to inhibit the release of cytochrome c and is involved in cell survival by preventing apoptosis. Survival Factors such as growth factors can also block apoptosis by activating signaling pathways that lead to the expression of anti-apoptotic proteins like Bcl2 or by inhibiting pro-apoptotic proteins. Conversely, the Fas ligand is a molecule expressed on cytotoxic T cells and NK cells that induces apoptosis by binding to the Fas molecule on a target cell, so it actually promotes the release of cytochrome c, rather than blocking it.

Answer 2

The I. Bcl2 protein would block the release of cytochrome c from mitochondria.

Step-by-step explanation:

The release of cytochrome c from mitochondria is a critical event in the intrinsic pathway of apoptosis, or programmed cell death. The I. Bcl2 protein is known to play a key regulatory role in this process. Bcl2, an anti-apoptotic protein, acts by inhibiting the permeabilization of the mitochondrial outer membrane, preventing the release of cytochrome c into the cytoplasm.

Survival factors and Fas ligand, on the other hand, are not directly involved in blocking the release of cytochrome c. Survival factors generally promote cell survival by activating signaling pathways that inhibit apoptosis.

Fas ligand, part of the extrinsic pathway of apoptosis, triggers cell death by binding to its receptor on the cell surface, leading to the activation of caspases. Neither of these factors is directly associated with preventing the release of cytochrome c from mitochondria.

Understanding the role of Bcl2 in inhibiting cytochrome c release provides insights into the intricate regulation of cell survival and death. Bcl2 achieves its anti-apoptotic effect by maintaining the integrity of the mitochondrial outer membrane. This knowledge is crucial for researchers studying apoptosis and can have implications for developing therapeutic strategies targeting this pathway in conditions where cell death regulation is disrupted. In conclusion, the Bcl2 protein is a key player in blocking the release of cytochrome c from mitochondria, preserving the cell's survival.