Retrotransposon-derived protein that forms virion-like capsids (PubMed:34413232). Acts as an effector of BAX during apoptosis: enriched at outer mitochondria membrane and associates with BAX upon induction of apoptosis, facilitating BAX-dependent mitochondrial outer membrane permeabilization and apoptosis (By similarity). Required for death receptor-dependent apoptosis (By similarity). When associated with RASSF1, promotes BAX conformational change and translocation to mitochondrial membranes in response to TNF and TNFSF10 stimulation (By similarity). Also promotes autophagy: promotes phagophore closure via association with ATG8 proteins (PubMed:33783314). Acts as an inhibitor of the NFE2L2/NRF2 pathway via interaction with SQSTM1: interaction promotes dissociation of SQSTM1 inclusion bodies that sequester KEAP1, relieving inactivation of the BCR(KEAP1) complex (By similarity). Homodimer. Under normal circumstances, held in an inactive conformation by an intramolecular interaction. Interacts with BAX. Binding to RASSF1 isoform A (RASSF1A) relieves this inhibitory interaction and allows further binding to BAX. Binds also to BCL2 and BCLX. Recruited to the TNFRSF1A and TNFRSF10A complexes in response to their respective cognate ligand, after internalization. Interacts with TRIM39 (By similarity). Interacts with RASSF6 (PubMed:17404571). Interacts with ATG8 proteins MAP1LC3A, MAP1LC3B and MAP1LC3C (By similarity). Does not interact with ATG8 proteins GABARAPL1, GABARAPL2 and GABARAP (By similarity). Interacts with SQSTM1; promoting dissociation of SQSTM1 inclusion bodies that sequester KEAP1 (By similarity). Forms virion-like extracellular vesicles that are released from cells. Widely expressed, including in the brain. High expression levels in testis. The protein is evolutionarily related to retrotransposon Gag proteins: it contains the capsid (CA)subdomain of gag. The BH3-like domain is required for association with BAX and for mediating apoptosis. The three BH domains (BH1, BH2, and BH3) of BAX are all required for mediating protein-protein interaction. The LIR motif (LC3-interacting region) is required for the interaction with the ATG8 family proteins MAP1LC3A, MAP1LC3B and MAP1LC3C. Ubiquitinated and degraded during mitotic exit by APC/C-Cdh1, this modification is inhibited by TRIM39. Belongs to the PNMA family.