Source:http://linkedlifedata.com/resource/pubmed/id/18471101
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2008-5-12
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pubmed:abstractText |
Our previous studies found that infectious pancreatic necrosis virus (IPNV) induces host apoptotic cell death, possibly through a newly synthesized protein trigger. Here, we examine whether IPNV infection can induce NF-kappaB activation through tyrosine kinase signalling of CHSE-214 cell death (host cell death). Using the electrophoretic mobility shift assay (EMSA) to detect transcription factor activation, we found that NF-kappaB is apparently activated 6-8 h post-IPNV infection. Using genistein (100 microg mL(-1); a tyrosine kinase inhibitor) to determine whether NF-kappaB activation requires tyrosine kinase activation, we found genistein blocks NF-kappaB activation at 8 h post-infection (p.i), and either enhances cell viability up to 50% at 12 h p.i. or blocks DNA fragmentation at 24 h p.i. Furthermore, the proteasome inhibitors PSI-I and PSI-II (both at 40 microm) also effectively blocked the NF-kappaB activation as well as stimulating a 30% increase in cell viability (30% decrease in apoptosis) at 8 and 12 h p.i. Taken together our data suggest that IPNV may induce NF-kappaB activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Genistein,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/benzyloxycarbonyl-isoleucyl-glutamyl...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0140-7775
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
451-60
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18471101-Animals,
pubmed-meshheading:18471101-Apoptosis,
pubmed-meshheading:18471101-Birnaviridae,
pubmed-meshheading:18471101-Birnaviridae Infections,
pubmed-meshheading:18471101-Cell Death,
pubmed-meshheading:18471101-Cell Line,
pubmed-meshheading:18471101-Cell Survival,
pubmed-meshheading:18471101-Cysteine Proteinase Inhibitors,
pubmed-meshheading:18471101-Fish Diseases,
pubmed-meshheading:18471101-Genistein,
pubmed-meshheading:18471101-NF-kappa B,
pubmed-meshheading:18471101-Oligopeptides,
pubmed-meshheading:18471101-Protein Kinase Inhibitors,
pubmed-meshheading:18471101-Protein-Tyrosine Kinases,
pubmed-meshheading:18471101-Salmon,
pubmed-meshheading:18471101-Signal Transduction,
pubmed-meshheading:18471101-Time Factors
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pubmed:year |
2008
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pubmed:articleTitle |
Aquatic birnavirus infection activates the transcription factor NF-kappaB via tyrosine kinase signalling leading to cell death.
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pubmed:affiliation |
Laboratory of Molecular Virology and Biotechnology, Institute of Biotechnology, National Cheng-Kung University, Tainan, Taiwan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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