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Vol. 59, Issue 4, 664-673, April 2001
Institute of Chemical Toxicology, Wayne State University, Detroit,
Michigan
The aryl hydrocarbon receptor (AhR) belongs to the basic
helix-loop-helix/periodicity/AhR nuclear translocator/simple-minded (Per-Arnt-Sim) family of transcription factors that regulate critical functions during development and tissue homeostasis. Within this family, the AhR is the only member conditionally activated in response
to ligand binding, typified by
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We recently
demonstrated that the AhR interacts with the retinoblastoma protein
(pRb). This report presents evidence that a LXCXE motif in the AhR
protein confers pRb binding, which is necessary for maximal TCDD
induced G1 arrest in rat 5L hepatoma cells. The data
support a mechanism whereby pRb seems to regulate G1 cell
cycle progression distinct from the direct repression of E2F-mediated
transcription. Furthermore, the results indicate that the AhR-pRb
interaction regulates TCDD induction of CYP1A1, suggesting that pRb may be a general AhR coactivator.
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