Evidences a(CHEBI:"amyloid-beta polypeptide 42") to p(HGNC:AK1)

Neuronal expression of AK1 is upregulated in AD patients and is induced by Ab42

Therefore, we examined whether oligomeric forms of Ab42 could regulate AK1 expression in neuronal cells.

From western blot analysis, we found that AK1 expression increased 􏰍2-fold in the cortical neurons after exposure to Ab42

As shown in Figure 5A and B, treatment of control cells with Ab42 reduced the levels of AMPK phosphorylation at Thr172 and the inhibitory phosphorylation of GSK3b at Ser9. On the contrary, these alterations triggered by Ab42 were not observed in SH-SY5Y/AK1 knockdown cells, showing no changes in the levels of the phosphorylated AMPK and GSK3b. These results suggest that AK1 plays a crucial role in the regulation of AMPK and GSK3b in the neuronal cells exposed to Ab42.

Compared with control neurons, the effects of Ab42 on tau phosphorylation at CP13, PHF-1 and AT180 epitopes were significantly ameliorated in AK1 knockdown cortical neurons

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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.