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Target intelligence / Profile preview
Fuzzy planar cell polarity protein (FUZ)
- Target
- FUZ
- Molecular classification
- Planar cell polarity effector, Ciliogenesis regulator, CPLANE complex protein, Other (not a receptor, enzyme, transporter, transcription factor, histone modifier, or ion channel)
01
Overview
Fuzzy planar cell polarity protein (FUZ) is a critical effector of planar cell polarity and ciliogenesis, functioning predominantly at the basal body of the primary cilium and regulating protein transport necessary for ciliary assembly. It has key roles in vertebrate embryonic development, especially neural and craniofacial patterning, through modulation of Hedgehog and Wnt/β-catenin signaling by ensuring correct ciliary function. Loss-of-function mutations lead to ciliopathy phenotypes, including neural tube defects, craniofacial abnormalities, and defective pituitary development, and in the nervous system, FUZ can induce apoptosis and contribute to neurodegeneration in polyglutamine diseases.
- Other names
- Protein fuzzy homologFYFLJ22688FyCPLANE3ciliogenesis and planar polarity effector complex subunit 3NTDfuzzy homologFUZ
02
Mechanism of action
Not applicable (no known drugs targeting FUZ; the protein acts via regulation of ciliary structure, PCP, and cell signaling, but is not a direct druggable target)
03
Biological functions
Ciliogenesis (formation and positioning of primary cilia)Planar cell polarity regulationSignal transduction (modulates Hedgehog and Wnt signaling)Apoptosis (induces neuronal apoptosis via specific signaling pathway)Cell movement and tissue morphogenesis
04
Disease associations
Neural tube defectsCraniofacial malformations (cleft palate, craniosynostosis)Pituitary gland development disordersPolyglutamine disease neurodegeneration (e.g., spinocerebellar ataxia type 3, Alzheimer's, Parkinson's)Short-rib polydactyly syndrome
05
Safety considerations
Mutations result in severe congenital abnormalities (embryonic lethality, craniofacial and skeletal defects, hypoplasia/regression of pituitary), which are inherent risks of FUZ dysfunction, not drug-related adverse effectsDisruption of FUZ can trigger pathogenic apoptosis in the nervous system
06
Interacting drugs
None known. No direct small molecule or clinical drug interaction is reported.
07
Biomarkers
No clinical biomarkers for patient selection or drug efficacy monitoring; molecular phenotype (ciliopathy, abnormal neural tube, etc.) could be used in genetic studies
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