p(MGI:Mapt, pmod(Ph, Ser, 199))
Here, we found that MG could induce tau hyperphosphorylation at multiple AD-related sites in neuroblastoma 2a cells under maintaining normal cell viability. MG treatment increased the level of advanced glycation end products (AGEs) and the receptor of AGEs (RAGE). PubMed:22798221
Taken all together, we think that activation of GSK-3b and p38 should be responsible for MG-induced tau hyperphosphorylation. PubMed:22798221
Taken all together, we think that activation of GSK-3b and p38 should be responsible for MG-induced tau hyperphosphorylation. PubMed:22798221
Western blot analyses of brain homogenates show that (-)-nilvadipine significantly reduces Tau phosphorylation in AT8 (phosphorylated Ser-199/Ser-202/Thr-205) and PHF-1 (phosphorylated Ser-396/Ser-404) epitopes (Fig. 3). PubMed:25331948
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.