Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1999-9-10
pubmed:abstractText
Human T lymphotropic virus type I trans-activator Tax protein regulates expression of several cellular genes that are involved in cellular activation, proliferation, and transformation. Tax mediates its regulatory activity through interaction with cellular transcription factors such as members of the cAMP-responsive element-binding factors/ATF family or the NF-kappaB/Rel family. In this study we have demonstrated that Tax trans-activates the promoter for CXCR4, a coreceptor for T cell-tropic HIV-1 through its association with nuclear respiratory factor 1 (NRF1). The promoter region for CXCR4 contains an NRF1-binding site, which is crucial for basal and Tax-induced activity. Glutathione S-transferase (GST) pull-down experiments showed association of GST-Tax fusion protein with NRF1 in vitro. Expression of Tax, in addition to stimulation with phorbol myristate acetate and ionomycin, increased formation of the NRF1 complex in a gel-mobility shift assay, indicating that Tax association with NRF1 in vivo facilitates its DNA binding. HTLV-I Tax activation of CXCR4 may contribute to the rapid progression of HIV disease observed in certain coinfected individuals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0889-2229
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
821-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
HTLV type I Tax activation of the CXCR4 promoter by association with nuclear respiratory factor 1.
pubmed:affiliation
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
pubmed:publicationType
Journal Article