Activation, myristolyation of BID and translocation to mitochondria

Stable Identifier
Homo sapiens
Activation of BID and translocation to mitochondria
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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).
Cleavage of BID to tBID can also be achieved by Granzyme B. The truncated protein is myristoylated and translocates to mitochondria.

Literature References
PubMed ID Title Journal Year
14634621 The Bcl-2 family: roles in cell survival and oncogenesis.

Cory, S, Huang, DC, Adams, JM

Oncogene 2003
9727492 Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

Li, H, Zhu, H, Xu, CJ, Yuan, J

Cell 1998
Participant Of
Event Information
Orthologous Events
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