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Figure 5.
Figure 5. IRF-3, KSHV IRF-1, TIF-2, and E1A Compete for
Binding to IBiD(A) CAT reporter activity measured in extracts of
cells transfected with the indicated plasmids (E1A 12S WT or
H3N: 1 μg; IRF-3 E5: 0.5 μg and 1 μg; KSHV IRF-1: 0.5 μg and
1 μg) or infected with Sendai virus.(B) In vitro pull-down
analysis using immobilized IBiD showing the competition for
binding to IBiD between TIF-2 (cold) and either IRF-3 E5 or KSHV
IRF-1 (^35S-labeled). The percentages of IRF-3 E5 and KSHV IRF-1
that remained bound are shown.(C) CAT assays showing the
inhibitory effect of either WT or H3N E1A 12S on virus induction
of (PRDIII-I)[3]. Amounts of effector constructs transfected:
0.5 and 1 μg. Immunoblot analysis (inset) using an α-E1A
antibody (Santa Cruz) indicates the expression levels of these
E1A constructs.(D) CAT assays showing the inhibitory effect of
either WT or H3N E1A 12S, and KSHV IRF-1 on the transcription
driven by Gal4-IRF-3 E5. Amounts of effector constructs
transfected: Gal4-IRF-3 E5, 50 ng; viral gene constructs, 0.25,
0.5, and 1 μg
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