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FLASH GENE

Symbol

APOA1

contributors: mct/npt - updated : 08-02-2019

HGNC name	apolipoprotein A-I
HGNC id	600

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type	restricted

constitutive of

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 Endocrine pancreas       moderately Lymphoid/Immune spleen       highly   thymus       moderately Reproductive male system seminal vesicles     moderately Visual eye anterior segment cornea

cell lineage
cell lines
fluid/secretion	plasma

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

isoforms

Precursor

secreted as a proprotein and then cleaved by an uncharacterized metalloproteinase

HOMOLOGY

interspecies

homolog to murine Apoa1 (65.91 pc)

Homologene

FAMILY

apolipoprotein A1/A4/E family

CATEGORY

regulatory , transport carrier

SUBCELLULAR LOCALIZATION	extracellular
	intracellular
	intracellular,cytoplasm,organelle,membrane
	intracellular,cytoplasm,organelle,endoplasmic reticulum ,rough,smooth

basic FUNCTION	involved in the reverse transport of cholesterol from tissues to liver
	both APOM and APOA1 mRNA may considered as independent risk factors for macrosomia

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

sensory transduction/vision

a component

INTERACTION

DNA

RNA

small molecule

protein	ABCA1 mediates unfolding the N terminus of APOA1 on the cell surface, followed by lipidation of APOA1 and release of nascent HDL
	ADRB3 might exert an anti-atherosclerotic effect by upregulating hepatic APOA1 expression and promoting the cholesterol reverse transport process

cell & other

REGULATION

Other

cleaved by BMP1 (cleaves human proapolipoprotein A1 and regulates its activation for lipid binding) (Chau 2007)

ASSOCIATED DISORDERS

corresponding disease(s)

NNHA , CCLD

Susceptibility

to premature atherosclerosis and to low HDL-cholesterol to premature coronary artery disease

Variant & Polymorphism other	deletion in exon 3 causing a frameshift and heterozygosity for a nucleotide substitution in exon 4 (T>G, L141R) increasing the risk of low HDL-cholesterol
	mutation L178P leads to endothelial dysfunction, increased arterial wall thickness, and premature coronary artery disease

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS