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Mitochondrial outer membrane permeabilization (MOMP), also known as the mitochondrial outer membrane permeability, is one of two ways apoptosis (a type of programmed cell death) can be activated. [1] It is part of the intrinsic pathway of apoptosis, also known as the mitochondrial pathway. MOMP is known as the point of no return in apoptosis.
The mitochondrial permeability transition pore (mPTP or MPTP; also referred to as PTP, mTP or MTP) is a protein that is formed in the inner membrane of the mitochondria under certain pathological conditions such as traumatic brain injury and stroke.
This defines a direct role for BAX in mitochondrial outer membrane permeabilization. BAX activation is stimulated by various abiotic factors, including heat, hydrogen peroxide, low or high pH, and mitochondrial membrane remodeling. In addition, it can become activated by binding BCL-2, as well as non-BCL-2 proteins such as p53 and Bif-1.
The Bcl-2 family proteins consists of members that either promote or inhibit apoptosis, and control apoptosis by governing mitochondrial outer membrane permeabilization (MOMP), which is a key step in the intrinsic pathway of apoptosis. A total of 25 genes in the Bcl-2 family were identified by 2008.
The mitochondria-associated ER membranes (MAMs), play role in cell death modulation. Mitochondrial outer membrane permeabilization (MOMP), is a reason of the higher matrix Ca 2+ levels, which is acts as a trigger for apoptosis. MOMP is the process before apoptosis, which is accompanied to permeability of the inner membrane of the mitochondria ...
This results in the release of cytochrome c and other pro-apoptotic factors (such as SMAC/DIABLO) [6] from the mitochondria, often referred to as mitochondrial outer membrane permeabilization, leading to activation of caspases. This defines BID as a direct activator of Bax, a role common to some of the pro-apoptotic Bcl-2 proteins containing ...
Moreover, BAK1 is believed to induce the opening of the mitochondrial voltage-dependent anion channel, leading to release of cytochrome c from the mitochondria. [6] Alternatively, BAK1 itself forms an oligomeric pore, MAC, in the MOM, through which pro-apoptotic factors leak in a process called MOM permeabilization. [9] [10] [11]
This gene is a member of the mitochondrial carrier subfamily of solute carrier protein genes. The product of this gene, adenine nucleotide translocator 2 (ANT2), functions as a major constituent of the mitochondrial permeability-transition pore complex that catalyzes the exchange of mitochondrial ATP with cytosolic ADP.