Figure 4.
Figure 4. Relationship between NF-κB activation and STAT1 or p53 activation in LCL cells. (A) Expression of STAT1 protein and levels of STAT1 tyrosine 701 phosphorylation in LCL cells transfected with pRT-1-IκBαS32,36A–inducible vector treated with (+) or without (-) doxycycline for 36 hours. (B) Expression of p53 protein and levels of p53 serine 15 phosphorylation in LCL cells transfected with pRT-1-IκBαS32,36A–inducible vector and pretreated with (+) or without (-) doxycycline for 36 hours. (C) CD95 mRNA expression by real-time RT-PCR (fold changes are indicated at the top of each bar compared with the untreated condition; error bars correspond to the standard deviation of 2 experiments) in LCL cells treated or not with the NF-κB inhibitor Bay11 in the presence or the absence of either IFNγ or fludarabine*.

Relationship between NF-κB activation and STAT1 or p53 activation in LCL cells. (A) Expression of STAT1 protein and levels of STAT1 tyrosine 701 phosphorylation in LCL cells transfected with pRT-1-IκBαS32,36A–inducible vector treated with (+) or without (-) doxycycline for 36 hours. (B) Expression of p53 protein and levels of p53 serine 15 phosphorylation in LCL cells transfected with pRT-1-IκBαS32,36A–inducible vector and pretreated with (+) or without (-) doxycycline for 36 hours. (C) CD95 mRNA expression by real-time RT-PCR (fold changes are indicated at the top of each bar compared with the untreated condition; error bars correspond to the standard deviation of 2 experiments) in LCL cells treated or not with the NF-κB inhibitor Bay11 in the presence or the absence of either IFNγ or fludarabine*.

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