rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
1999-9-10
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pubmed:abstractText |
In this study, we have investigated the ability of insulin-like growth factor I (IGF-I) to inhibit HIV long terminal repeat (LTR)-driven gene expression. Using COS 7 cells cotransfected with tat and an HIV LTR linked to a chloramphenicol acetyltransferase (CAT) reporter, we observed that physiological levels of IGF-I (10(-9) M) significantly inhibited CAT expression in a concentration- and time-dependent manner. IGF-I did not inhibit CAT expression in COS 7 cells transfected with pSVCAT, and did not affect CAT expression in the absence of cotransfection with tat. Transfection of HIV-1 proviral DNA into COS 7 cells +/- IGF-I resulted in a significant decrease (p < 0.05) in infectious virion production. Both IGF-I and Ro24-7429 inhibited LTR-driven CAT expression, while TNF-alpha-enhanced CAT expression was not affected by IGF-I. On the other hand, a plasmid encoding parathyroid hormone-related peptide exhibited dramatic additivity of inhibition of CAT expression in COS 7 cells. Finally, we show that in Jurkat or U937 cells cotransfected with HIVLTRCAT/tat, IGF-I significantly inhibited CAT expression. Further, interleukin 4 showed in U937 cells inhibition of CAT expression that was not additive to IGF-I induced inhibition. Our data demonstrate that IGF-I can specifically inhibit HIVLTRCAT expression. This inhibition may occur at the level of the tat/TAR interaction. Finally, this IGF-I effect is seen in target cell lines and similar paths of inhibition may be involved in the various cell types employed.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-HIV Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Benzodiazepines,
http://linkedlifedata.com/resource/pubmed/chemical/Chloramphenicol O-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tat,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Reverse Transcriptase,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/PTHLH protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone-Related Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrroles,
http://linkedlifedata.com/resource/pubmed/chemical/Ro 24-7429,
http://linkedlifedata.com/resource/pubmed/chemical/tat Gene Products, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0889-2229
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
10
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
829-36
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10381171-Animals,
pubmed-meshheading:10381171-Anti-HIV Agents,
pubmed-meshheading:10381171-Benzodiazepines,
pubmed-meshheading:10381171-COS Cells,
pubmed-meshheading:10381171-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:10381171-Gene Expression Regulation, Viral,
pubmed-meshheading:10381171-Gene Products, tat,
pubmed-meshheading:10381171-Genes, Reporter,
pubmed-meshheading:10381171-HIV Long Terminal Repeat,
pubmed-meshheading:10381171-HIV Reverse Transcriptase,
pubmed-meshheading:10381171-HIV-1,
pubmed-meshheading:10381171-Humans,
pubmed-meshheading:10381171-Insulin-Like Growth Factor I,
pubmed-meshheading:10381171-Interleukin-4,
pubmed-meshheading:10381171-Jurkat Cells,
pubmed-meshheading:10381171-Parathyroid Hormone-Related Protein,
pubmed-meshheading:10381171-Proteins,
pubmed-meshheading:10381171-Pyrroles,
pubmed-meshheading:10381171-U937 Cells,
pubmed-meshheading:10381171-tat Gene Products, Human Immunodeficiency Virus
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pubmed:year |
1999
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pubmed:articleTitle |
Effect of insulin-like growth factor I on HIV type 1 long terminal repeat-driven chloramphenicol acetyltransferase expression.
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pubmed:affiliation |
Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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