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. 2002 Jul 29;99(16):10736–10741. doi: 10.1073/pnas.112338099

Fig 1.

Fig 1.

Increased NF-κB activation and IFN-β production in delNS1 virus-infected A549 cells results in activation of target genes. (A) Electrophoretic mobility-shift assay analysis of NF-κB binding to its cognate DNA element. An oligonucleotide corresponding to the NF-κB binding site was labeled with 32P and incubated with nuclear extracts from mock-infected or virus-infected A549 cells at 16 h postinfection, as indicated. Cells were also infected with Sendai virus as a positive control of this experiment. The position of the NF-κB/DNA complex is shown. (B) Northern blot analysis of IFN-β and cellular genes with known NF-κB or IFN responsive elements. A β-actin control Northern is also shown. The moi and the postinfection times that were used in these experiments are indicated on the top. The average fold change and P value observed by microarray analysis at 8 h postinfection of repeated experiments is shown on the right. The IFN-β gene was not present on microarrays used (N/A). The asterisk indicates the microarray results for α-actin because the β-actin cDNA was not represented on the array. It should be noted that, in contrast to some other cell lines, such as MDCK cells, no severe cytopathic effect was induced in A549 cells after influenza virus infection.