Pathway
Activation, myristolyation of BID and translocation to mitochondria
BID may promote cell death by activating BAX and BAK while inactivating anti-apoptotic proteins. The engagement of cell surface receptors activates the caspase-8, a heterodimer, that cleaves BID in its amino terminal region. This particular event may act as a link between Extrinsic (caspase 8/10 dependent) and Intrinsic (Bcl-2 inhibitable) pathways although some evidences from mouse genetic experiments suggest the contrary. It has been suggested that the death signals from the extrinsic or death receptor pathway may get amplified by the mechanisms of intrinsic pathway and that this functional loop may be enabled by the molecules like tBID (truncated BID).
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Cleavage of BID to tBID can also be achieved by Granzyme B. The truncated protein is myristoylated and translocates to mitochondria.
What the reference databases state
Statements
4 statements
4 statements · 1 reference database · Subject: Activation, myristolyation of BID and translocation to mitochondria · Sources: Reactome
- BID participates in Activation, myristolyation of BID and translocation to mitochondriaProteinReactome R-HSA-75108Inferred only
- CASP8 participates in Activation, myristolyation of BID and translocation to mitochondriaProteinReactome R-HSA-75108Inferred only
- GZMB participates in Activation, myristolyation of BID and translocation to mitochondriaProteinReactome R-HSA-75108Inferred only
- NMT1 participates in Activation, myristolyation of BID and translocation to mitochondriaProteinReactome R-HSA-75108Inferred only