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Phospholipid-transporting ATPase VA (ATP10A)
- Target
- ATP10A
- Molecular classification
- Enzyme, Transporter, P-type ATPase (specifically P4-ATPase family)
01
Overview
Phospholipid-transporting ATPase VA (ATP10A) is a catalytic component of the P4-ATPase flippase complex, functioning as an ATP-dependent phospholipid translocase and crucial for maintaining plasma membrane lipid asymmetry, particularly by flipping phosphatidylcholine from the outer to the inner leaflet of the membrane. This activity is central to modulating membrane dynamics, affecting cell morphology, adhesion, and spreading, and is also implicated in cell signaling and internalization of specific proteins. ATP10A may be involved in neurodevelopmental and metabolic disorders, with epigenetic modifications at the locus correlating with differential metabolic outcomes. Its genetic localization within the chromosome 15q11–13 region links it to Angelman syndrome when deleted or altered[1][2][3]
- Other names
- ATP10AATP10CATPVAATPVCATPase class V type 10Aaminophospholipid translocase VAP4-ATPase flippase complex alpha subunit ATP10Aphospholipid-transporting ATPase VAKIAA0566
02
Mechanism of action
Enzymatic hydrolysis of ATP linked to inward translocation ("flipping") of phosphatidylcholine and related phospholipids from outer to inner leaflet of plasma membrane[1][3] Alters lipid composition to affect cell shape, signaling, and membrane curvature
03
Biological functions
Maintenance of plasma membrane lipid asymmetryTranslocation ("flipping") of phospholipids (especially phosphatidylcholine, and to a lesser extent, phosphatidylserine and phosphatidylethanolamine)Modulation of cell morphology, size, adhesion, and spreadingMembrane dynamics and cell signalingCell trafficking
04
Disease associations
Neurodevelopmental disorders (e.g., Angelman syndrome due to effect in 15q11–13 region)[2][3][1]Potential metabolic regulation/obesity (epigenetic roles)[1]Potential roles in cell adhesion-related pathologies
05
Safety considerations
Potential genetic imprinting or deletion effects in 15q11–13 associated with Angelman syndrome, suggesting developmental and neurological risk if disrupted[2][3][1]Loss-of-function changes may affect cell membrane composition, morphogenesis, and signal transduction
06
Biomarkers
Differential DNA methylation at ATP10A locus correlated with metabolic response (e.g., to hypocaloric diet), possible use in obesity/metabolic biomarker studies[1]
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