Bcl2 Interacting Killer, Apoptosis Inducing (BIK)

Bcl-2-interacting killer is known to interact with cellular and viral survival-promoting proteins, such as BCL2 and the Epstein-Barr virus in order to enhance programed cell death. Because its activity is suppressed in the presence of survival-promoting proteins, this protein is suggested as a likely target for antiapoptotic proteins. This protein shares a critical BH3 domain with other death-promoting proteins, BAX and BAK.

This death-promoting activity of BIK was suppressed by coexpression of BCL2, BCLXL, EBV BHRF1, and E1B 19-kD, suggesting that BIK may be a common target for antiapoptotic proteins. The predicted 160-amino acid BIK protein contains a C-terminal hydrophobic domain, a characteristic shared by BCL2 family members.