Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-10-12
pubmed:abstractText
The facts that fibronectin (FN) mRNA is elevated in cells expressing human T cell leukemia virus type I (HTLV-I) Tax protein and that Tax is known to transactivate the cellular cAMP-response element (CRE) prompted us to examine whether Tax activates the FN promoter of which CRE is thought to play an important role. We showed that Tax transactivated the FN promoter in Jurkat cells. Deletion analyses showed that the response-element resides within the promoter region of -69 bp and that an NF-kappaB-binding site at -41 bp is involved in the Tax-activation of the FN promoter. Gel-shift assays showed that DNA-protein complexes binding to the NF-kappaB site, composed of NF-kappaB p50/p65, were induced on the NF-kappaB motif at -41 bp by Tax. Overexpression of NF-kappaB enhanced the Tax-activation of the FN promoter. Our study shows that the FN promoter is transactivated by Tax through the NF-kappaB pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
276
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
579-86
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Transactivation of fibronectin promoter by HTLV-I Tax through NF-kappaB pathway.
pubmed:affiliation
Department of Biochemistry, School of Medicine, Kyungpook National University, 101 Dongin-dong, Jung-gu, Taegu, 700-422, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't