p(FPLX:AKT, pmod(Ph, Ser, 473))

Entity

Name

AKT

Namespace

FPLX

Namespace Version

20180917

Namespace URL

https://raw.githubusercontent.com/sorgerlab/famplex/e8ae9926ff95266032cb74f77973c84939bffbeb/export/famplex.belns

Tau Modifications Sections of NESTOR

We found a significant increase in brain AKT Ser473 phosphorylation (T-test, P<0.001) and GSK3β Ser9 phosphorylation (T-test, P<0.001) in Tg Tau P301S mice treated with anatabine. Figure 11. DOI:10.4172/2168-975X.1000126

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

We found that treatment of SH-SY5Y cells with BAY61-3606 inhibits AKT phosphorylation (Fig. 9, A and B), which is consistent with previous studies (59) investigating the impact of Syk inhibition on AKT activation. PubMed:25331948

GSK3β is inactivated upon phosphorylation of Ser9 by protein kinase B (AKT) [41] whereas AKT phosphorylation at Ser473 results in AKT activation [42]. DOI:10.4172/2168-975X.1000126

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

Phosphorylation at Thr-308 and Ser-473 leads to activation of Akt and it was found that deregulation of Akt is associated with various human malignancies. PubMed:23454242