Accelerates programmed cell death. Association to the apoptosis repressors Bcl-X(L), BHRF1, Bcl-2 or its adenovirus homolog E1B 19k protein suppresses this death-promoting activity. Does not interact with BAX. Interacts with RHBDL4/RHBDD1 (PubMed:18953687). Interacts with BCL2L10/BCL-B (PubMed:23235460, PubMed:23563182). Around the nuclear envelope, and in cytoplasmic membranes. Intact BH3 motif is required by BIK, BID, BAK, BAD and BAX for their pro-apoptotic activity and for their interaction with anti-apoptotic members of the Bcl-2 family. Proteolytically cleaved by RHBDL4/RHBDD1. RHBDL4/RHBDD1-induced cleavage is a necessary step prior its degradation by the proteosome-dependent mechanism.