|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
1
|
|
pubmed:dateCreated |
1997-1-31
|
|
pubmed:abstractText |
The caprine arthritis-encephalitis virus (CAEV) long terminal repeat (LTR) is activated by gamma interferon (IFN-gamma) in promonocytic cells. We have previously shown that a 70-bp element is necessary and sufficient for the response of the CAEV LTR to this cytokine. At the 5' end, this 70-bp IFN-gamma response element contains sequence similarity to the gamma activated site (GAS). Here we demonstrate that the putative GAS element in the CAEV LTR binds specifically to a cellular factor induced by IFN-gamma in promonocytic cells. Substitution mutations in this consensus sequence eliminate binding of the inducible factor. The GAS element from the 70-bp motif is sufficient to confer responsiveness to IFN-gamma using a heterologous minimal promoter. Consistent with the binding data, the same mutations in the GAS element eliminate responsiveness to IFN-gamma in the context of both a functional CAEV LTR and a heterologous promoter. The cellular factor that binds to the GAS element is present from 5 min to 14 h after stimulation with IFN-gamma. Binding of the nuclear factor to the GAS element in the CAEV LTR is inhibited by antibody directed against STAT1 (p91/84). Thus, the GAS sequence in the CAEV LTR is essential for the response to IFN-gamma and a STAT1-like factor binds to this site. The STAT-1 signaling pathway provides at least one mechanism for activation of the CAEV LTR by IFN-gamma in monocytes. These data are the first demonstration of a role for a STAT family member in the regulation of a viral promoter.
|
|
pubmed:grant |
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-1326822,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-2425264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-2552171,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-2654643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-2824834,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-3021973,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-3126690,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-3855947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-6153243,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-6409419,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7507205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7526796,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7543024,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7574495,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7696211,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7796299,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-7914891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8016643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8139015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8197455,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8200035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8456300,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8510231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8523577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8590733,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8608586,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8608597,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8608598,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8985415-8628285
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jan
|
|
pubmed:issn |
0022-538X
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
71
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
771-7
|
|
pubmed:dateRevised |
2009-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:8985415-Arthritis-Encephalitis Virus, Caprine,
pubmed-meshheading:8985415-Base Sequence,
pubmed-meshheading:8985415-DNA, Viral,
pubmed-meshheading:8985415-DNA-Binding Proteins,
pubmed-meshheading:8985415-Humans,
pubmed-meshheading:8985415-Intercellular Adhesion Molecule-1,
pubmed-meshheading:8985415-Interferon-alpha,
pubmed-meshheading:8985415-Molecular Sequence Data,
pubmed-meshheading:8985415-Monocytes,
pubmed-meshheading:8985415-Nuclear Proteins,
pubmed-meshheading:8985415-Repetitive Sequences, Nucleic Acid,
pubmed-meshheading:8985415-STAT1 Transcription Factor,
pubmed-meshheading:8985415-Signal Transduction,
pubmed-meshheading:8985415-Time Factors,
pubmed-meshheading:8985415-Trans-Activators,
pubmed-meshheading:8985415-Tumor Cells, Cultured
|
|
pubmed:year |
1997
|
|
pubmed:articleTitle |
STAT1 pathway is involved in activation of caprine arthritis-encephalitis virus long terminal repeat in monocytes.
|
|
pubmed:affiliation |
Department of Medicine, University of California-San Francisco, 94121, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|
