Mitochondrial control of apoptosis refers to the critical role played by mitochondria in regulating the intrinsic mechanism of apoptosis. The intrinsic pathway of apoptosis is a tightly regulated system that ultimately eliminates unwanted or damaged cells. It plays essential roles in normal development, tissue homeostasis, and the elimination of potentially harmful cells, such as those with irreparable DNA damage or excessive cellular stress. The key players in mitochondrial control of apoptosis are the Bcl-2 family proteins: the Bcl-2 family are composed of both pro-apoptotic and anti-apoptotic members with the balance between these two groups critical in determining whether a cell will undergo apoptosis. Anti-apoptotic members, such as Bcl-2 and Bcl-xL prevent the release of cytochrome c from the intermembrane space of the mitochondria, thereby inhibiting apoptosis. In contrast, pro-apoptotic members such as Bax and Bak, promote cytochrome c release and trigger apoptosis. During apoptosis, the key event for pro-apoptotic signals is inducing the permeabilization of the outer mitochondrial membrane, leading to the release of cytochrome c and other factors into the cytoplasm. The permeabilization occurs via two main mechanisms, one involving Bcl-2 family members, the other via opening of the Mitochondrial Permeability Transition Pore (MPTP) a non-specific pore that spans the inner and outer mitochondrial membranes. The MTPT is a large protein complex, which includes the voltage-dependent anion channel (VDAC) in the outer membrane, the adenine nucleotide translocator (ANT) in the inner membrane, and cyclophilin D in the matrix. When apoptosis is triggered, pro-apoptotic Bcl-2 family proteins, particularly Bax and Bak, undergo conformational changes and translocate to the outer mitochondrial membrane. There they form oligomers that create pores in the mitochondrial membrane that allow the release of proteins that are normally confined to the intermembrane space, such as cytochrome c. The MPTP can be triggered to open by various signals, such as elevated levels of calcium ions, oxidative stress, and increased levels of reactive oxygen species (ROS). When the MPTP opens, it causes an increase in the permeability of the inner mitochondrial membrane, leading to the collapse of the mitochondrial membrane potential and the release of several factors from the intermembrane space into the cytoplasm. In addition to cytochrome c, other pro-apoptotic factors, such as Smac/DIABLO (Second mitochondrial-derived activator of caspases/Direct IAP Binding Protein with Low pI) and AIF (Apoptosis-Inducing Factor), can also be released through the MPTP. These factors also contribute to the activation of caspases and induce chromatin condensation and DNA fragmentation, further promoting apoptosis. We offer a comprehensive product range of research reagents for studying mitochondrial control of apoptosis, including Raf1 antibodies, Prohibitin antibodies, Cytochrome C antibodies, Raf1 ELISA Kits, and APAF1 ELISA Kits. Explore our full mitochondrial control of apoptosis product range below and discover more, for less.