Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-3
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
199-207
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Ah receptor signals cross-talk with multiple developmental pathways.
pubmed:affiliation
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
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't