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Bcl-xL

B-cell lymphoma-extra large (Bcl-xl, or BCL2-like 1 isoform 1) is a transmembrane molecule in the mitochondria. It is a member of the Bcl-2 family of proteins, and acts as a pro-survival protein by preventing the release of mitochondrial contents such as cytochrome c, which would lead to caspase activation. It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins define whether the cell will undergo cell death: if more Bcl-xL is present, then pores are non-permeable to pro-apoptotic molecules and the cell survives. However, if Bax and Bak become activated, and Bcl-xL is sequestered away by gatekeeper BH3-only factors (e.g. Bim), causing a pore to form, cytochrome c is released leading to initiation of caspase cascade leading to apoptotic events.

Bcl-xL functions at the level of intrinsic apoptotic pathway, while extrinsic pathway ( Fas/ TNF death receptors) directly leads to caspase activation. There is a link between extrinsic and intrinsic pathways, via caspase-mediated cleavage of BID, which functions to activate pore formation at the mitochondria.