PUBLICATION

Covalent Modification and Regulation of the Nuclear Receptor Nurr1 by a Dopamine Metabolite

Authors
Bruning, J.M., Wang, Y., Oltrabella, F., Tian, B., Kholodar, S.A., Liu, H., Bhattacharya, P., Guo, S., Holton, J.M., Fletterick, R.J., Jacobson, M.P., England, P.M.
ID
ZDB-PUB-190312-4
Date
2019
Source
Cell chemical biology   26(5): 674-685.e6 (Journal)
Registered Authors
Guo, Su, Oltrabella, Francesca
Keywords
5,6-dihydroxyindole, 5,6-dihydroxyindolequinone, 5,6-indolequinone, DHI, DHICA, IQ, Nr4A2, Nurr1, Parkinson's disease, cysteine adduct, dopamine homeostasis, dopamine metabolite, dopamine oxidation, ligand-binding domain, ligand-binding pocket, nuclear receptor, nuclear receptor related 1 protein, redox sensor
MeSH Terms
  • Animals
  • Zebrafish/growth & development
  • Zebrafish/metabolism
  • Crystallography, X-Ray
  • Indoles/chemistry
  • Indoles/metabolism*
  • Indoles/pharmacology
  • Thermodynamics
  • Protein Domains
  • Nuclear Receptor Subfamily 4, Group A, Member 2/chemistry
  • Nuclear Receptor Subfamily 4, Group A, Member 2/genetics
  • Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism*
  • Binding Sites
  • Molecular Dynamics Simulation
  • Cell Line, Tumor
  • Oxidative Stress/drug effects
  • Larva/metabolism
  • Humans
  • Dopamine/chemistry
  • Dopamine/metabolism*
  • Recombinant Proteins/biosynthesis
  • Recombinant Proteins/chemistry
  • Recombinant Proteins/genetics
  • Transcription, Genetic/drug effects
PubMed
30853418 Full text @ Cell Chem Biol
Abstract
Nurr1, a nuclear receptor essential for the development, maintenance, and survival of midbrain dopaminergic neurons, is a potential therapeutic target for Parkinson's disease, a neurological disorder characterized by the degeneration of these same neurons. Efforts to identify Nurr1 agonists have been hampered by the recognition that it lacks several classic regulatory elements of nuclear receptor function, including the canonical ligand-binding pocket. Here we report that the dopamine metabolite 5,6-dihydroxyindole (DHI) binds directly to and modulates the activity of Nurr1. Using biophysical assays and X-ray crystallography, we show that DHI binds to the ligand-binding domain within a non-canonical pocket, forming a covalent adduct with Cys566. In cultured cells and zebrafish, DHI stimulates Nurr1 activity, including the transcription of target genes underlying dopamine homeostasis. These findings suggest avenues for developing synthetic Nurr1 ligands to ameliorate the symptoms and progression of Parkinson's disease.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping