Selected-GenAtlas references	SOURCE	GeneCards	NCBI Gene	Swiss-Prot	Ensembl
	HGNC	UniGene	Nucleotide	OMIM	UCSC

Home Page

FLASH GENE

Symbol

MOAP1

contributors: mct - updated : 05-09-2018

HGNC name	modulator of apoptosis 1
HGNC id	16658

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

DNA

TYPE	functioning gene
STRUCTURE	2.71 kb     3 Exon(s)

10 Kb 5' upstream gene genomic sequence study

MAPPING

cloned

Y

linked

N

status

provisional

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_022151 3 - 2435 NP_071434 - 351 - 2009 19100260

EXPRESSION

Type	ubiquitous

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Cardiovascular heart       highly Endocrine pancreas         Nervous brain hindbrain cerebellum       brain       highly Skin/Tegument skin         Urinary kidney

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Epithelial secretory glandular endocrine   Muscular striatum skeletal

cell lineage
cell lines	retinoblastoma
fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	a BH3-like motif
	C-terminal region associated with the death domain of TNFRSF1A

mono polymer

homomer , dimer

HOMOLOGY

Homologene

FAMILY

PNMA family

CATEGORY

tumor suppressor

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,organelle,mitochondria,outer
	intracellular,cytoplasm,organelle,membrane
	intracellular,cytoplasm,cytosolic
text	mitochondria-enriched protein
	MOAP1 is a BAX-binding protein enriched at the outer mitochondrial membrane (OMM)

basic FUNCTION	mediates caspase-dependent apoptosis
	is a direct mitochondrial target of BAX
	apoptotic stimuli can facilitate the proapoptotic function of BAX in mitochondria through stabilization of MOAP1
	association of RASSF1 and MOAP1 with death receptors involves an ordered recruitment to receptor complexes to promote cell death and inhibit tumor formation
	is a BH3-like protein that plays key roles in cell death or apoptosis
	role for MOAP1 in FAS signaling in the liver by promoting MTCH2-mediated BID recruitment to mitochondria
	pro-apoptotic tumor suppressor molecule with a growing set of known interacting partners

CELLULAR PROCESS	cell life, cell death/apoptosis

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein	interacts with BCL2 and BCL-XL
	BAX-associating protein (MOAP1 may act as an effector for promoting BAX function in mitochondria)
	binding TNFRSF1A (association domains on both MOAP1 and RASSF1 were essential for death receptor-dependent apoptosis)
	TRIM39-binding protein (extends the half-life of MOAP1 by inhibiting its poly-ubiquitination process)
	MOAP1 is a novel substrate of the anaphase-promoting complex (APC/C(Cdh1)) ubiquitin ligase
	influence of TRIM39 on MOAP1 levels stems from the ability of TRIM39 (a RING domain E3 ligase) to directly inhibit APC/C(Cdh1)-mediated protein ubiquitylation
	is an integral partner to the tumor suppressor protein, (RASSF1), and functions to activate the BCL2 family pro-apoptotic protein BAX
	PNMA2 functions as antagonist of MOAP1 and PNMA1 through heterodimeric interaction
	BAX-binding protein enriched at the outer mitochondrial membrane (OMM)
	PNMA5 interacts with MOAP1 and N-terminal domain of PNMA5 is required for interaction with MOAP1
	robust association with RACK1, a versatile scaffolding protein that responds to activation of protein kinase C

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   sensitizes cells to apoptotic stimuli and promotes recombinant BAX-mediated cytochrome c release from isolated mitochondria

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

Moap-1-deficient mice are resistant to Fas-induced hepatocellular apoptosis and lethality