%0 Figure %A Hoenen, Claire %A Gustin, Audrey %A Birck, Cindy %A Kirchmeyer, Mélanie %A Beaume, Nicolas %A Felten, Paul %A Grandbarbe, Luc %A Heuschling, Paul %A Heurtaux, Tony %D 2016 %T A53T protein induces NFkB, AP-1 and Nrf2 recruitment. %U https://plos.figshare.com/articles/figure/A53T_protein_induces_NFkB_AP-1_and_Nrf2_recruitment_/3828144 %R 10.1371/journal.pone.0162717.g007 %2 https://plos.figshare.com/ndownloader/files/5973546 %K 30P %K PD %K Lewy bodies causes dopaminergic %K synuclein %K wild-type %K Alpha-Synuclein Proteins Promote Pro-Inflammatory Cascades %K point mutations %K E 46K exposure %K protein %K 53T microglial reactivity mechanism %K MAPK %X

Nuclear localization of the p65 subunit, c-Fos (subunit of AP-1) as well as Nrf2 was evaluated on microglial cells after a 5 μM A53T exposure for 30 min, 1 h or 2 h (Fig 7A). These chemiluminescent detection assays were realized by western-blot with 10 μg of nuclear proteins. The histone deacetylase 1 (HDAC1) was used as a loading control. Furthermore, p65, c-Fos and Nrf2 detected proteins were normalized and quantified (Fig 7B). Results are given as mean ± SEM of at least three independent experiments. * p < 0.05, ** p < 0.01, significantly different from control condition. A cytoplasmic protein negative control western-blot (αTub) was also realized (Fig 7C) to demonstrate the effectiveness of the nuclear isolation.

%I PLOS ONE