期刊
JOURNAL OF FISH DISEASES
卷 31, 期 6, 页码 451-460出版社
WILEY
DOI: 10.1111/j.1365-2761.2008.00928.x
关键词
apoptosis; infectious pancreatic necrosis virus; NF-kappa B; proteasome inhibitors PSI-I and II; tyrosine kinase inhibitor genistein
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-kappa B 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-kappa B is apparently activated 6-8 h post-IPNV infection. Using genistein (100 mu g mL(-1); a tyrosine kinase inhibitor) to determine whether NF-kappa B activation requires tyrosine kinase activation, we found genistein blocks NF-kappa B 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 mu M) also effectively blocked the NF-kappa B 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-kappa B activation through tyrosine kinase signalling, which may be associated with induction of apoptosis.
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