Target intelligence / Profile preview

Phospholipase A and acyltransferase 3 (PLAAT3)

Target
PLAAT3
Molecular classification
Enzyme, Phospholipase (specifically group XVI PLA2), Acyltransferase
01

Overview

Phospholipase A and acyltransferase 3 (PLAAT3) is a group XVI phospholipase A2 enzyme with both phospholipase and acyltransferase activities, predominantly located in the cytoplasm and associated with cellular membranes. It preferentially hydrolyzes phosphatidylcholines, regulates lipid homeostasis in white adipose tissue, and plays critical roles in adipocyte differentiation, organelle degradation, and cellular responses to viral entry. In human disease, PLAAT3 is implicated in hereditary lipodystrophy with neurological manifestations and is a potential drug target for obesity and metabolic syndrome. Its roles in cancer and microbial infection are complex, exhibiting both tumor suppressive and promoting activities, and facilitating or restricting viral genome entry depending on the context[1][2][3][4][5].

Other names
HRASLS3HREV107PLA2G16AdPLAH-REV107adipose-specific phospholipase A2Group XVI phospholipase A2Renal carcinoma antigen NY-REN-65H-rev 107 protein homologHRAS-like suppressor 3FPLD9phospholipase A/acyltransferase-3Ca-independent phospholipase A1/2adipose-specific PLA2
02

Mechanism of action

Drugs or interventions that silence or inhibit PLAAT3 likely decrease pathological lipolysis and alter adipocyte differentiation, beneficial in metabolic syndrome. Modulation of PLAAT3 may affect viral genome delivery or clearance during picornavirus infection.

03

Biological functions

Lipid metabolism (hydrolyzes phosphatidylcholines at sn-2 position, releases fatty acids, catalyzes N-acyltransferase reaction)Modulates adipocyte function and differentiation (dependent on PPARγ signaling)Host factor for viral infection (picornaviruses, hepatitis A)Potential tumor suppressor or facilitator (contrasting reports in cancer)Cellular membrane remodeling, organelle degradation (e.g. during lens cell differentiation)
04

Disease associations

Metabolic syndrome and obesity (potential protective role against diet-induced obesity in mice)Lipodystrophy (hereditary form with neurological manifestations)Cancer (both suppressor and promoter roles reported)Microbial infection (host factor in picornavirus infection, restriction in hepatitis A infection)Acute flaccid myelitis (allied disease association)
05

Safety considerations

Loss-of-function variants lead to lipodystrophy and neurological symptoms (demyelinating neuropathy, intellectual disability), associated with metabolic complicationsPotential for unintended effects on lipid metabolism and viral susceptibility
06

Interacting drugs

thiazolidinediones

1 more in the full profile.

07

Biomarkers

PLAAT3 is identified as a biomarker for seminomaIts deficiency correlates with decreased PPARγ signaling as a marker of adipocyte dysfunction

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