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FLASH GENE

Symbol

APOO

contributors: mct - updated : 22-11-2017

HGNC name	apolipoprotein O
HGNC id	28727

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type

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 Digestive liver       highly Homo sapiens Lymphoid/Immune tonsils       highly

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

HOMOLOGY

Homologene

FAMILY

apolipoprotein O family

CATEGORY

DNA associated

SUBCELLULAR LOCALIZATION	extracellular
	plasma membrane
	intracellular
	intracellular,cytoplasm,organelle,mitochondria,inner
	intracellular,cytoplasm,organelle,membrane
	intracellular,cytoplasm,organelle,endoplasmic reticulum
	intracellular,cytoplasm,organelle,Golgi
text	three distinct forms: (1) a glycosylated and secreted 55kDa protein, (2) an ER/Golgi-resident form thereof, and (3) a non-glycosylated 22kDa mitochondrial protein

basic FUNCTION	apolipoprotein that is present predominantly in high density lipoprotein (HDL)
	represents a link between impaired mitochondrial function and cardiomyopathy onset
	APOO and APOOL, regulate their levels in an antagonistic manner
	in liver enhances likely hepatic lipid accumulation by impairing mitochondrial function
	is linked to cardiolipin metabolism and promotes crista junction formation

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component	CHCHD6, APOOL and APOO appear to be periphery subunits of the MICOS complex, because their depletion does not affect cristae morphology or stability of other components
	APOO and APOOL were suggested to represent constituents of the mammalian Mitofilin/MINOS complex

INTERACTION

DNA

RNA

small molecule

protein

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   overexpression of APOO induced fragmentation of mitochondria, promoted ROS formation and resulted in impaired mitochondrial respiration constitutional     --low   depletion led to alterations in mitochondrial ultrastructure and caused a significant reduction in the number of crista junctions

Susceptibility

Variant & Polymorphism

Candidate gene
Marker	may be regarded as an independent inflammatory predictor of acute coronary syndrome (ACS) patients
Therapy target
	System Type Disorder Pubmed cardiovascular cardiomyopathy   targeting APOO-dependent metabolic remodeling has potential as a strategy to adjust heart metabolism and protect the myocardium from impaired contractility

ANIMAL & CELL MODELS