Target intelligence / Profile preview

Phospholipid phosphatase-related protein type 1 (PLPPR1)

Target
PLPPR1
Molecular classification
Other (integral membrane signaling modulator), Plasticity-related gene (PRG) family member, Lipid phosphatase-related protein (inactive phosphatase; lacks full enzymatic activity)
01

Overview

Phospholipid phosphatase-related protein type 1 (PLPPR1) is an integral membrane protein belonging to the plasticity-related gene (PRG) family, predominantly expressed in the brain[1][2][3]. Unlike classical lipid phosphatases, PLPPR1 is catalytically inactive but plays a major signaling-modulatory role. It promotes filopodia formation, supports neurite outgrowth, and modulates neuronal plasticity by attenuating RhoA/ROCK and Rac1 signaling, primarily through physical interaction with RhoGDI1. PLPPR1 is crucial for neuronal development, axon guidance, synaptic plasticity, and may help overcome inhibitory environments (e.g., chondroitin sulfate proteoglycans and LPA), thus supporting neuroregeneration after injury[1][2]. Its unique function is to stabilize actin cytoskeleton dynamics and regulate cell adhesion, influencing brain development and response to damage, but it is not currently a direct target of any approved therapeutic drugs[1][2][3][4].

Other names
Plasticity-related gene 3 proteinPRG-3PRG3Lipid phosphate phosphatase-related protein type 1Inactive 2-lysophosphatidate phosphatase PLPPR1LPPR1MGC26189FLJ20300
02

Mechanism of action

Not established for drug action; endogenous mechanism: attenuation of RhoA/ROCK and Rac1 signaling via binding to RhoGDI1—decreases actinomyosin contractility and stabilizes growth/APG structures[1][2].

03

Biological functions

Regulation of cytoskeletal dynamicsNeurite outgrowth and plasticityInhibition of RhoA and Rac1 signalingFilopodia formationCell adhesion modulationImpairment of lysophosphatidic acid (LPA)-induced neurite retractionPotential modulation of neuronal development and regeneration
04

Disease associations

Neuroregenerative processes (supports axon regeneration, adult neurogenesis, enhances functional recovery after CNS injury)Potential implications in cancer cell adhesion/migration and metastasis (based on family members, strongest for the nervous system)
05

Safety considerations

None described in the literature; unknown safety or toxicity profile in humans or preclinical models. Main challenge: lack of detailed mechanistic/therapeutic data and uncertain off-target consequences of modulation
06

Interacting drugs

None known or reported in public literature as of this time
07

Biomarkers

None established for patient selection or efficacy monitoring

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