a(CHEBI:"dimethyl fumarate")

Entity

Name

dimethyl fumarate

Namespace

chebi

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Wild-type MEFs treated with DMF (20 μM) showed a time-dependent response effect activating phosphorylation of ERK (Fig. 2A, B) and p38 (Fig. 2A, C), that was maximal within 5 min. The Ser/Thr protein kinase AKT, an upstream regulator of GSK-3β, was also activated after 5 min as determined by increased phosphorylation of S473 (Fig. 2A, D) PubMed:29121589

Taken together, our results show that DMF reduces GSK-3 activity in vivo as determined by a significant and subtle reduction in the phosphorylation levels of its two substrates TAU and CRMP2 respectively. PubMed:29121589

Wild-type MEFs treated with DMF (20 μM) showed a time-dependent response effect activating phosphorylation of ERK (Fig. 2A, B) and p38 (Fig. 2A, C), that was maximal within 5 min. The Ser/Thr protein kinase AKT, an upstream regulator of GSK-3β, was also activated after 5 min as determined by increased phosphorylation of S473 (Fig. 2A, D) PubMed:29121589

Wild-type MEFs treated with DMF (20 μM) showed a time-dependent response effect activating phosphorylation of ERK (Fig. 2A, B) and p38 (Fig. 2A, C), that was maximal within 5 min. The Ser/Thr protein kinase AKT, an upstream regulator of GSK-3β, was also activated after 5 min as determined by increased phosphorylation of S473 (Fig. 2A, D) PubMed:29121589

Wild-type MEFs treated with DMF (20 μM) showed a time-dependent response effect activating phosphorylation of ERK (Fig. 2A, B) and p38 (Fig. 2A, C), that was maximal within 5 min. The Ser/Thr protein kinase AKT, an upstream regulator of GSK-3β, was also activated after 5 min as determined by increased phosphorylation of S473 (Fig. 2A, D) PubMed:29121589

DMF increased the phosphorylation levels of GSK-3βSer9 in both genotypes, indicating that this effect is upstream of NRF2 as shown in Fig. 3A. PubMed:29121589

Taken together, our results show that DMF reduces GSK-3 activity in vivo as determined by a significant and subtle reduction in the phosphorylation levels of its two substrates TAU and CRMP2 respectively. PubMed:29121589

Taken together, our results show that DMF reduces GSK-3 activity in vivo as determined by a significant and subtle reduction in the phosphorylation levels of its two substrates TAU and CRMP2 respectively. PubMed:29121589

Astrocytes displayed enlarged bodies and ramifications (Type B morphology), consistent with a reactive state after TAUP301L expression in Nrf2+/+ and Nrf2−/− mice (Fig. 6A left panels). However, only astrocytes from Nrf2+/+ mice treated with DMF were maintained in a resting morphology (Type A) (Fig. 6A right panels). Concerning microglia, TAUP301L expression induced a very significant increase in IBA1+ microglia at the ipsilateral hippocampal side of Nrf2+/+ and Nrf2−/− mice (Fig. 7A), which was confirmed by stereological quantification (Fig. 7B). DMF treatment reduced significantly this microgliosis in Nrf2+/+ but not in Nrf2−/− mice, reinforcing the idea of NRF2-dependent anti-inflammatory effect PubMed:29121589

Astrocytes displayed enlarged bodies and ramifications (Type B morphology), consistent with a reactive state after TAUP301L expression in Nrf2+/+ and Nrf2−/− mice (Fig. 6A left panels). However, only astrocytes from Nrf2+/+ mice treated with DMF were maintained in a resting morphology (Type A) (Fig. 6A right panels). Concerning microglia, TAUP301L expression induced a very significant increase in IBA1+ microglia at the ipsilateral hippocampal side of Nrf2+/+ and Nrf2−/− mice (Fig. 7A), which was confirmed by stereological quantification (Fig. 7B). DMF treatment reduced significantly this microgliosis in Nrf2+/+ but not in Nrf2−/− mice, reinforcing the idea of NRF2-dependent anti-inflammatory effect PubMed:29121589

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

The greatest FImax was observed with Protandim at 135-fold, followed by bardoxolone methyl at 67-fold, dimethyl fumarate at 55-fold, and sulforaphane at 21-fold PubMed:22020111

When compared contemporaneously in the AREc32-based assay, FImax observed was in the order Protandim > bardoxolone methyl > dimethyl fumarate > sulforaphane. PubMed:22020111

A recent laboratory study of dimethyl fumarate found that the compound activates Nrf2 in primary astrocytes, but not in the C6 glioma-derived cell line (Wilms et al., 2010), demonstrating that different cells may respond quite differently to Nrf2 activators PubMed:22020111

A recent laboratory study of dimethyl fumarate found that the compound activates Nrf2 in primary astrocytes, but not in the C6 glioma-derived cell line (Wilms et al., 2010), demonstrating that different cells may respond quite differently to Nrf2 activators PubMed:22020111

While Protandim, bardoxolone methyl, BG-12, and sulforaphane all have been demonstrated to modify gene expression profiles by activation of Nrf2, they have not been compared side by side, in the same cell line, under identical conditions. PubMed:22020111