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- Bc21a557fd87dfc681bd301011601b8bd NCIT_P378 "BIOCARTA" @default.
- Bc21a557fd87dfc681bd301011601b8bd type Axiom @default.
- Bc21a557fd87dfc681bd301011601b8bd annotatedProperty NCIT_P325 @default.
- Bc21a557fd87dfc681bd301011601b8bd annotatedSource NCIT_C39154 @default.
- Bc21a557fd87dfc681bd301011601b8bd annotatedTarget "Mitochondria participate in apoptotic signaling pathways through the release of mitochondrial proteins into the cytoplasm. Cytochrome c, a key protein in electron transport, is released from mitochondria in response to apoptotic signals, and activates Apaf-1, a protease released from mitochondria. Activated Apaf-1 activates caspase-9 and the rest of the caspase pathway. Smac/DIABLO is released from mitochondria and inhibits IAP proteins that normally interact with caspase-9 to inhibit apoptosis. Apoptosis regulation by Bcl-2 family proteins occurs as family members form complexes that enter the mitochondrial membrane, regulating the release of cytochrome c and other proteins. TNF family receptors that cause apoptosis directly activate the caspase cascade, but can also activate Bid, a Bcl-2 family member, which activates mitochondria-mediated apoptosis. Bax, another Bcl-2 family member, is activated by this pathway to localize to the mitochondrial membrane and increase its permeability, releasing cytochrome c and other mitochondrial proteins. Bcl-2 and Bcl-xL prevent pore formation, blocking apoptosis. AIF (apoptosis inducing factor) is another mitochondrial factor that is released into the cytoplasm to induce apoptosis. AIF-induced apoptosis is important during development but is not caspase dependent. (This definition may be outdated - see the DesignNote.)" @default.