Linked Life Data

15282404

Source:http://linkedlifedata.com/resource/pubmed/id/15282404

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-10-19
pubmed:abstractText
ZfAHR2 has been identified as the receptor that is essential for mediating the developmental toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in zebrafish. One form of zfARNT2, zfARNT2b, forms a functional heterodimer with zfAHR2 that specifically recognizes XREs in gel shift experiments and induces XRE-driven transcription in COS-7 cells treated with TCDD. However, it has not been demonstrated that zfARNT2b acts as the physiological dimerization partner for zfAHR2 to mediate TCDD toxicity in developing zebrafish. An antisense morpholino targeted against zfARNT2 (zfarnt2-MO) along with a line of mutant zebrafish lacking expression of the zfarnt2 gene have been used to test the hypothesis that zfARNT2 mediates the developmental toxicity of TCDD. Injection of the zfarnt2-MO decreased expression of the zfARNT2 protein but did not provide any protection against the formation of pericardial edema at 72 hpf. In addition, in TCDD dose response studies the zfarnt2(-/-) embryos showed no protection against three endpoints of TCDD toxicity observed at 96 hpf: pericardial edema, reduced trunk blood flow, and shortened lower jaw. Finally, immunostaining results at 96 hpf demonstrate that the zfarnt2(-/-) embryos show a similar pattern of TCDD-induced zfCYP1A expression as WT embryos. These results demonstrate that zfARNT2 is not essential for mediating TCDD developmental toxicity in zebrafish and suggest that alternate dimerization partner(s) exist for zfAHR2 in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1096-6080
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
250-8
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:15282404-Abnormalities, Drug-Induced, pubmed-meshheading:15282404-Animals, pubmed-meshheading:15282404-Animals, Genetically Modified, pubmed-meshheading:15282404-Aryl Hydrocarbon Receptor Nuclear Translocator, pubmed-meshheading:15282404-Dose-Response Relationship, Drug, pubmed-meshheading:15282404-Embryo, Nonmammalian, pubmed-meshheading:15282404-Gene Expression Regulation, Developmental, pubmed-meshheading:15282404-Morpholines, pubmed-meshheading:15282404-Oligodeoxyribonucleotides, Antisense, pubmed-meshheading:15282404-Receptors, Aryl Hydrocarbon, pubmed-meshheading:15282404-Teratogens, pubmed-meshheading:15282404-Tetrachlorodibenzodioxin, pubmed-meshheading:15282404-Toxicity Tests, pubmed-meshheading:15282404-Transcription Factors, pubmed-meshheading:15282404-Zebrafish, pubmed-meshheading:15282404-Zebrafish Proteins
pubmed:year
2004
pubmed:articleTitle
ARNT2 is not required for TCDD developmental toxicity in zebrafish.
pubmed:affiliation
Molecular and Environmental Toxicology Center, and School of Pharmacy, University of Wisconsin, 77 Highland Avenue, Madison, WI 53705, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.