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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1990-2-16
|
| pubmed:abstractText |
Despite continuing controversies related to public policy, information on the molecular biology of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has advanced significantly over the past decade. Current understanding of the biological mechanisms of TCDD action is based upon the interactions of TCDD with a genetically expressed cytosolic macromolecule that functions as a receptor in many cells across many species. The Ah receptor recognizes TCDD and structurally similar molecules and serves as the transducing step whereby TCDD alters gene expression through the association of the TCDD:receptor complex with specific TCDD-responsive elements on the genome. Understanding these molecular events and their relevance to the organ-level manifestations of TCDD toxicity may be critical to formulating scientifically based assessments of the risk of TCDD exposure.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0271-3586
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
16
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
455-74
|
| pubmed:dateRevised |
2006-2-27
|
| pubmed:meshHeading | |
| pubmed:year |
1989
|
| pubmed:articleTitle |
Dioxins and the Ah receptor.
|
| pubmed:affiliation |
Toxic Chemicals Program, Environmental Defense Fund, Washington, DC 20036.
|
| pubmed:publicationType |
Journal Article,
Review
|