BID的活化、棕榈酰化及转位至线粒体
中文名称
通路描述
BID可能通过激活BAX和BAK促进细胞死亡，同时抑制抗凋亡蛋白。细胞表面受体的结合激活caspase-8，这是一种异二聚体，其亚氨基末端切割BID。这一事件可能作为外源（依赖caspase-8/10）和内源（可被Bcl-2抑制）通路之间的桥梁，尽管一些来自小鼠遗传实验的证据表明相反。外源或死亡受体途径的信号可能通过内源途径的机制得到放大，这种功能回路可能由分子如tBID（截短的BID）所启用。Granzyme B也可将BID切割为tBID，截短蛋白被棕榈酰化并转位至线粒体。
英文描述
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). Cleavage of BID to tBID can also be achieved by Granzyme B. The truncated protein is myristoylated and translocates to mitochondria.
所含基因
4 个基因