MOAP1

The protein encoded by this gene was identified by its interaction with apoptosis regulator BAX protein. This protein contains a Bcl-2 homology 3 (BH3)-like motif, which is required for the association with BAX. When overexpressed, this gene has been shown to mediate caspase-dependent apoptosis. [provided by RefSeq, Jul 2008]

Modulator Of Apoptosis 1

Retrotransposon-derived protein that forms virion-like capsids (By similarity).

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 (PubMed:11060313, PubMed:16199525).

Required for death receptor-dependent apoptosis (PubMed:11060313).

When associated with RASSF1, promotes BAX conformational change and translocation to mitochondrial membranes in response to TNF and TNFSF10 stimulation (PubMed:15949439).

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 (PubMed:33393215).

Apoptotic signaling pathway Source: BHF-UCL
Extrinsic apoptotic signaling pathway in absence of ligand Source: BHF-UCL
Extrinsic apoptotic signaling pathway via death domain receptors Source: BHF-UCL
Intrinsic apoptotic signaling pathway in response to DNA damage Source: BHF-UCL
Positive regulation of apoptotic process Source: UniProtKB
Positive regulation of autophagosome assembly Source: UniProtKB
Positive regulation of release of cytochrome c from mitochondria Source: BHF-UCL
Protein insertion into mitochondrial membrane involved in apoptotic signaling pathway Source: BHF-UCL
Regulation of apoptotic process Source: GO_Central

Mitochondrion
Mitochondrion outer membrane
cytosol 1 Publication
Other locations
Extracellular vesicle membrane
Note: Forms virion-like extracellular vesicles that are released from cells.

Ubiquitinated and degraded during mitotic exit by APC/C-Cdh1, this modification is inhibited by TRIM39.