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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: NF-κB transcriptional activation by TNFα requires phospholipase C, extracellular signal-regulated kinase 2 and poly(ADP-ribose) polymerase-1

Fig. 7

ERK2-mediated phosphorylation of PARP-1 induces NF-κB transcriptional activity. a NF-κB transcriptional activity was evaluated in astrocytes transfected with a reporter gene in which dEGFP expression (green) is driven by NF-κB p65 subunit binding. TNFα-induced (15 ng/ml). dEGFP expression is blocked by the PARP-1 inhibitor, DPQ (25 μM). Scale bar, 20 μm. Quantified data are shown in c. (*p < 0.05 compared to control, # p < 0.05 compared to TNFα, n = 3–4). b TNFα-induced GFP expression is absent in PARP1−/− astrocytes and reconstituted in PARP-1−/− astrocytes transfected with normal human PARP-1 (wt PARP-1) but not with mutant S372A and T372A PARP-1, which lacks ERK2 phosphorylation sites. Conversely, PARP-1−/− astrocytes transfected with mutant S372E PARP-1, which has a phosphomimetic glutamate residue at an ERK2 phosphorylation site, show increased basal NF-κB transcriptional activation. Scale bar, 10 μm. Quantified data are shown in d. (*p < 0.05 compared to wt PARP-1, n = 3). Expression levels of the mutant PARP-1 species were comparable, as evaluated by PARP-1 western blots using a polyclonal antibody (not shown)

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