Target intelligence / Profile preview

ATPase phospholipid-transporting 9B (ATP9B)

Target
ATP9B
Molecular classification
Enzyme, Transporter, P4-ATPase (phospholipid flippase)
01

Overview

ATPase phospholipid-transporting 9B (ATP9B) is a member of the P4-ATPase family, functioning as an ATP-dependent phospholipid "flippase" that translocates specific phospholipids from the exoplasmic to the cytoplasmic leaflet of cellular membranes[1][2][4]. Unlike most other P4-ATPases, ATP9B localizes to the trans-Golgi network and can exit the endoplasmic reticulum independently of CDC50 proteins[2][4]. ATP9B forms homo- or heteromeric complexes (notably with ATP9A) to mediate efficient vesicular trafficking, particularly in exocytic pathways between the Golgi and plasma membrane[4]. The gene is implicated in certain neurodevelopmental and hepatic disorders, and polymorphisms may modulate susceptibility to additional conditions such as skin diseases, but ATP9B is not currently a direct drug target, nor are clinically approved drugs known to interact with it[1][2][4].

Other names
Probable phospholipid-transporting ATPase IIBATPIIBNEO1LHUSSY-20ATPASEPhMMR1Macrophage MHC receptor 1Putative phospholipid-transporting ATPase IIB
02

Mechanism of action

Not applicable or none known (no known targeting drugs as of current evidence)

03

Biological functions

Phospholipid translocation ("flipping" phospholipids between membrane leaflets)Maintenance of membrane lipid asymmetryRetrograde vesicle-mediated transport (Golgi to endoplasmic reticulum)EndocytosisExocytic membrane trafficking (Golgi to plasma membrane)
04

Disease associations

Neurodevelopmental disorders (e.g., cerebellar ataxia, impaired intellectual development, and dysequilibrium syndrome)Progressive familial intrahepatic cholestasisPossibly skin disorders (e.g., Hailey-Hailey disease, as a genetic modifier)
05

Safety considerations

Not explicitly described; theoretical risks based on family include disruption of membrane trafficking and lipid homeostasis with potential neurologic or hepatic consequences if inhibited

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