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rdf:type |
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lifeskim:mentions |
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026844,
umls-concept:C0132555,
umls-concept:C0205263,
umls-concept:C0205548,
umls-concept:C0805732,
umls-concept:C1135918,
umls-concept:C1150611,
umls-concept:C1335960,
umls-concept:C1366753,
umls-concept:C1548425,
umls-concept:C1704259,
umls-concept:C1705987
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pubmed:issue |
2
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pubmed:dateCreated |
1998-12-30
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pubmed:abstractText |
Inducible nitric oxide synthase (iNOS) is induced in many cell types by cytokines and lipopolysaccharide (LPS). Cytokine signal transduction is believed to be mediated primarily through the JAK/STAT pathway. We therefore examined the effects of a JAK2-specific inhibitor, an antisense oligonucleotide to JAK2, and electroporation of neutralizing anti-STAT1 and anti-STAT3 antibodies on IFNgamma- and LPS-stimulated induction of iNOS in vascular smooth muscle cells. Unexpectedly, we found that the JAK/STAT pathway suppresses IFNgamma- and LPS-stimulated iNOS induction in these cells. In contrast, the JAK/STAT pathway appears to have a positive role in iNOS induction in RAW 264.7 macrophages.
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pubmed:grant |
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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/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Jak2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0006-291X
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 1998 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
18
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pubmed:volume |
252
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
508-12
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9826561-Animals,
pubmed-meshheading:9826561-Base Sequence,
pubmed-meshheading:9826561-Cells, Cultured,
pubmed-meshheading:9826561-DNA-Binding Proteins,
pubmed-meshheading:9826561-Enzyme Induction,
pubmed-meshheading:9826561-Interferon-gamma,
pubmed-meshheading:9826561-Janus Kinase 2,
pubmed-meshheading:9826561-Lipopolysaccharides,
pubmed-meshheading:9826561-Muscle, Smooth, Vascular,
pubmed-meshheading:9826561-Nitric Oxide Synthase,
pubmed-meshheading:9826561-Nitric Oxide Synthase Type II,
pubmed-meshheading:9826561-Oligodeoxyribonucleotides,
pubmed-meshheading:9826561-Protein-Tyrosine Kinases,
pubmed-meshheading:9826561-Proto-Oncogene Proteins,
pubmed-meshheading:9826561-Rats,
pubmed-meshheading:9826561-Recombinant Proteins,
pubmed-meshheading:9826561-STAT1 Transcription Factor,
pubmed-meshheading:9826561-STAT3 Transcription Factor,
pubmed-meshheading:9826561-Signal Transduction,
pubmed-meshheading:9826561-Trans-Activators
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pubmed:year |
1998
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pubmed:articleTitle |
Inhibition by the JAK/STAT pathway of IFNgamma- and LPS-stimulated nitric oxide synthase induction in vascular smooth muscle cells.
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pubmed:affiliation |
Vascular Biology Center, Medical College of Georgia, Augusta, Georgia, 30912, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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