Source:http://linkedlifedata.com/resource/pubmed/id/11297551
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
25
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pubmed:dateCreated |
2001-6-18
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pubmed:abstractText |
The sedative and anti-nausea drug thalidomide, which causes birth defects in humans, has been shown to have both anti-inflammatory and anti-oncogenic properties. The anti-inflammatory effect of thalidomide is associated with suppression of cytokine expression and the anti-oncogenic effect with inhibition of angiogenesis. It is presently unclear whether the teratogenic properties of thalidomide are connected in any way to the beneficial, anti-disease characteristics of this drug. The transcription factor NF-kappaB has been shown to be a key regulator of inflammatory genes such as tumor necrosis factor-alpha and interleukin-8. Inhibition of NF-kappaB is associated with reduced inflammation in animal models, such as those for rheumatoid arthritis. We show here that thalidomide can block NF-kappaB activation through a mechanism that involves the inhibition of activity of the IkappaB kinase. Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2. These data indicate that the therapeutic potential for thalidomide may be based on its ability to block NF-kappaB activation through suppression of IkappaB kinase activity.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CHUK protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Probes,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/IKBKB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IKBKE protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Thalidomide,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
276
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
22382-7
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11297551-Base Sequence,
pubmed-meshheading:11297551-DNA Probes,
pubmed-meshheading:11297551-Enzyme Inhibitors,
pubmed-meshheading:11297551-Gene Expression Regulation,
pubmed-meshheading:11297551-Humans,
pubmed-meshheading:11297551-I-kappa B Kinase,
pubmed-meshheading:11297551-Interleukin-1,
pubmed-meshheading:11297551-Interleukin-8,
pubmed-meshheading:11297551-Jurkat Cells,
pubmed-meshheading:11297551-NF-kappa B,
pubmed-meshheading:11297551-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11297551-Thalidomide,
pubmed-meshheading:11297551-Transcription, Genetic,
pubmed-meshheading:11297551-Tumor Necrosis Factor-alpha
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pubmed:year |
2001
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pubmed:articleTitle |
Inhibition of NF-kappa B activity by thalidomide through suppression of IkappaB kinase activity.
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pubmed:affiliation |
Curriculum in Genetics and Molecular Biology, the Department of Biology, and the Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599-7295, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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