PUBLICATION

AHR-dependent misregulation of Wnt signaling disrupts tissue regeneration

Authors
Mathew, L.K., Simonich, M.T., and Tanguay, R.L.
ID
ZDB-PUB-081028-7
Date
2009
Source
Biochemical pharmacology   77(4): 498-507 (Review)
Registered Authors
Mathew, Lijoy K., Tanguay, Robyn L.
Keywords
none
MeSH Terms
  • Animals
  • Extremities/physiology
  • Humans
  • Models, Biological
  • Receptors, Aryl Hydrocarbon/genetics
  • Receptors, Aryl Hydrocarbon/metabolism
  • Receptors, Aryl Hydrocarbon/physiology*
  • Regeneration/genetics
  • Regeneration/physiology*
  • Reproduction/drug effects
  • Reproduction/physiology
  • Signal Transduction*
  • Wnt Proteins/genetics
  • Wnt Proteins/metabolism*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish/physiology
PubMed
18938144 Full text @ Biochem. Pharmacol.
Abstract
The origins of molecular toxicology can be traced to understanding the interactions between halogenated aromatic hydrocarbons and the aryl hydrocarbon receptor (AHR). The physiological consequences of activation of the aryl hydrocarbon receptor are diverse, and we are just beginning to understand the importance of the AHR signal transduction pathway in homeostasis and disease. The many downstream targets that mediate these biological responses remain undefined. Studies have exploited the power of the zebrafish model to elucidate the mechanisms by which AHR activation disrupts biological signaling. Recent genomic analysis performed in a zebrafish tissue regeneration model revealed functional cross talk between AHR and the well-established Wnt/beta-catenin signal transduction pathway. This review focuses on the development of the zebrafish model of AHR biology and the application of in vivo toxicogenomics to unravel molecular mechanisms.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping