Target intelligence / Profile preview

Adhesion G protein-coupled receptor F4 (ADGRF4)

Target
ADGRF4
Molecular classification
G protein-coupled receptor, Adhesion receptor, Seven-transmembrane receptor, Transmembrane protein
01

Overview

Adhesion G protein-coupled receptor F4 (ADGRF4), also known as GPR115 or PGR18, is a member of the adhesion G protein-coupled receptor (GPCR) family, structurally characterized by a large extracellular N-terminus and seven transmembrane domains[1][2][7]. ADGRF4 is an "orphan" receptor, meaning its endogenous ligand is not known, but it can be activated by synthetic peptides derived from related family members[7]. ADGRF4 is classified within the adhesion class (Family VI) of GPCRs and is distinguished from most other AGPCRs by lacking a canonical GPCR autoproteolysis-inducing (GAIN) domain and GPS motif, which means it does not undergo autoproteolysis like classical AGPCRs[2]. In mouse models, this receptor is implicated in proper enamel mineralization by ameloblasts, but knockout does not cause general developmental anomalies, and its role in human disease is not well defined[1][7]. Rare associations have been made with complex cortical dysplasia, but its physiological ligand, pharmacology, and implications as a drug target remain poorly characterized[1][7].

Other names
GPR115PGR18FLJ38076probable G-protein coupled receptor 115G-protein coupled receptor PGR18
02

Mechanism of action

No approved or well-characterized drugs; agonist activity demonstrated for synthetic peptides derived from the "Stachel sequence" of ADGRF5, indicating capacity for G protein (Gq/G11) signaling[7]

03

Biological functions

Signal transductionCell adhesionTransmembrane signaling receptor activity
04

Disease associations

Possible role in brain malformations (specifically "Cortical dysplasia, complex, with other brain malformations 14A")Dental enamel mineralization disorder (mouse data)
05

Safety considerations

No specific safety concerns or therapeutic challenges documented; knockout mice show no gross developmental or fertility defects[7]

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