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Fig. 2 | Molecular Brain

Fig. 2

From: Ubiquilin-2 drives NF-κB activity and cytosolic TDP-43 aggregation in neuronal cells

Fig. 2

hUBQLN2 expression in Neuro2A cells caused cellular stress via MAP kinase pathway. a Cytoplasmic (C) and nuclear (N) extraction was realized 48 h after transfection. Neuro2A cells were treated with TNF-α 20 ng/ml for 4 h. b Hypothetical model of NF-κB activation by hUBQLN2. p38 MAPK seems to be a major player in this activation. c Quantification of cytosolic phospho-p42/44 MAPK vs non-phosphorylated p42/44 MAPK (p = phospho)(n = 3), (d) cytosolic phospho-p38 vs non-phosphorylated p38 MAPK (p = 0.0051 for hUBQLN2WT and p < 0.05 for hUBQLN2P497H, n = 3) and (e) cytosolic phospho-JNK vs non-phosphorylated JNK MAPK (n = 3) as compared to cytoplasmic level in control cells. f Neuro2A cells were pre-treated 1 h with MAPK inhibitors 10 μM U0126-EtOH, SB203580, SP600125 and then treated with TNF-α 20 ng/ml for 4 h. Total protein extract was used for analysis. g Luciferase assay showing control plasmid, pCMV-hUBQLN2WT and pCMV-hUBQLN2P497H transfected Neuro2A cells. Cells were pre-treated 1 h with MAPK inhibitors 10 μM U0126-EtOH, SB203580, SP600125 and then treated with TNF-α 20 ng/ml for 4 h (n = 3). h Previous (g) luciferase activity was calculated in percentage of control Neuro2A cells, treated with SB203580 or not

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