PMID- 15627472
OWN - NLM
STAT- MEDLINE
DCOM- 20050218
LR  - 20071114
IS  - 0006-2952 (Print)
IS  - 0006-2952 (Linking)
VI  - 69
IP  - 2
DP  - 2005 Jan 15
TI  - Ah receptor signals cross-talk with multiple developmental pathways.
PG  - 199-207
AB  - For many years, the Ah receptor (AHR) has been a favorite of toxicologists and 
      molecular biologists studying the connections between genes and the changes in 
      the control of gene expression resulting from environmental exposures. Much of 
      the attention given to the Ah receptor has focused on the nature of its ligands, 
      many of which are known or suspected carcinogens, and on the role that its best 
      studied regulatory product, the CYP1A1 enzyme, plays in toxic responses and 
      carcinogen activation. This understandable bias has resulted in a 
      disproportionate amount of Ah receptor research being directed at toxicological 
      or adaptive end points. In recent times, it has become evident that Ah receptor 
      functions are also involved in molecular cascades that lead to inhibition of 
      proliferation, promotion of differentiation, or apoptosis, with an important 
      bearing in development. Developmental and toxicological AHR functions may not 
      always be related. The ancestral AHR protein in invertebrates directs the 
      developmental fate of a few specific neurons and does not bind xenobiotic 
      ligands. The mammalian AHR maintains normal liver function in the absence of 
      exogenous ligands and, when activated by dioxin, cross-talks with morphogenetic 
      and developmental signals. Toxic end points, such as the induction of cleft 
      palate by dioxin in mice embryos, might be at the crossroads of these signals and 
      provide important clues as to the developmental role of the AHR.
FAU - Puga, Alvaro
AU  - Puga A
AD  - Center for Environmental Genetics and Department of Environmental Health, 
      University of Cincinnati Medical Center, P.O. Box 670056, Cincinnati, OH 
      45267-0056, USA. alvaro.puga@uc.edu
FAU - Tomlinson, Craig R
AU  - Tomlinson CR
FAU - Xia, Ying
AU  - Xia Y
LA  - eng
GR  - 1R01 ES10708/ES/NIEHS NIH HHS/United States
GR  - 1R01 ES11798/ES/NIEHS NIH HHS/United States
GR  - 2R01 ES06273/ES/NIEHS NIH HHS/United States
GR  - P30 ES06096/ES/NIEHS NIH HHS/United States
GR  - P42 ES04908/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
DEP - 20040927
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (Receptors, Aryl Hydrocarbon)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation, Developmental/drug effects/physiology
MH  - Humans
MH  - Receptor Cross-Talk/*physiology
MH  - Receptors, Aryl Hydrocarbon/*physiology
MH  - Signal Transduction/drug effects/*physiology
RF  - 114
EDAT- 2005/01/04 09:00
MHDA- 2005/02/19 09:00
CRDT- 2005/01/04 09:00
PHST- 2004/05/06 00:00 [received]
PHST- 2004/06/02 00:00 [accepted]
PHST- 2005/01/04 09:00 [pubmed]
PHST- 2005/02/19 09:00 [medline]
PHST- 2005/01/04 09:00 [entrez]
AID - S0006-2952(04)00460-5 [pii]
AID - 10.1016/j.bcp.2004.06.043 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 2005 Jan 15;69(2):199-207. doi: 10.1016/j.bcp.2004.06.043. 
      Epub 2004 Sep 27.