Disrupting the DNA Binding of EGR-1 with a Small-Molecule Inhibitor Ameliorates 2,4-Dinitrochlorobenzene-Induced Skin Inflammation

J Invest Dermatol. 2021 Jul;141(7):1851-1855. doi: 10.1016/j.jid.2020.12.029. Epub 2021 Feb 4.
No abstract available

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • DNA / metabolism*
  • Dermatitis, Atopic / chemically induced
  • Dermatitis, Atopic / drug therapy*
  • Dermatitis, Atopic / immunology
  • Dermatitis, Atopic / pathology
  • Dinitrochlorobenzene / administration & dosage
  • Dinitrochlorobenzene / toxicity
  • Disease Models, Animal
  • Early Growth Response Protein 1 / antagonists & inhibitors*
  • Early Growth Response Protein 1 / genetics
  • Early Growth Response Protein 1 / metabolism
  • HaCaT Cells
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Mice
  • Mice, Knockout
  • Molecular Docking Simulation
  • Protein Binding / drug effects
  • THP-1 Cells
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Dinitrochlorobenzene
  • EGR1 protein, human
  • Early Growth Response Protein 1
  • Egr1 protein, mouse
  • TNF protein, human
  • Tnf protein, mouse
  • Tumor Necrosis Factor-alpha
  • DNA