p(HGNC:AK1)

Entity

Name

AK1

Namespace

hgnc

Namespace Version

20180906

Namespace URL

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

Neuronal expression of AK1 is upregulated in AD patients and is induced by Ab42 PubMed:22419736

Therefore, we examined whether oligomeric forms of Ab42 could regulate AK1 expression in neuronal cells. PubMed:22419736

From western blot analysis, we found that AK1 expression increased 􏰍2-fold in the cortical neurons after exposure to Ab42 PubMed:22419736

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. PubMed:22419736

AK1 expression also increased in neuronal cells which were exposed to oxidative stress but not to other toxic insults, such as proteostasis stressors PubMed:22419736

AK1 also increased in the hippocampus of APP-J20, an AD model mouse expressing familial AD-mutant APP (Supple- mentary Material, Fig. S1A and B). PubMed:22419736

the AK1 level was higher in the hippocampus of 9-, 12- and 15-month-old Tg2576 mice expressing Swedish mutant of amyloid precursor protein (hAPP) PubMed:22419736

Neuronal expression of AK1 is upregulated in AD patients and is induced by Ab42 PubMed:22419736

With the immunohisto- chemical analysis, we found that the expression levels of AK1 markedly elevated in the NeuN-positive hippocampal neurons of AD patients PubMed:22419736

the AK1 level was higher in the hippocampus of 9-, 12- and 15-month-old Tg2576 mice expressing Swedish mutant of amyloid precursor protein (hAPP) PubMed:22419736

AK1 also increased in the hippocampus of APP-J20, an AD model mouse expressing familial AD-mutant APP (Supple- mentary Material, Fig. S1A and B). PubMed:22419736

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 PubMed:22419736

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. PubMed:22419736

Ectopic expression of AK1 in mouse cortical neurons increased immunoreactivity against phosphorylated tau at Ser396/404 (PHF-1), Ser202 (CP13) and Ser231/Thr235 (AT180) PubMed:22419736

Ectopic expression of AK1 in mouse cortical neurons increased immunoreactivity against phosphorylated tau at Ser396/404 (PHF-1), Ser202 (CP13) and Ser231/Thr235 (AT180) PubMed:22419736

Ectopic expression of AK1 in mouse cortical neurons increased immunoreactivity against phosphorylated tau at Ser396/404 (PHF-1), Ser202 (CP13) and Ser231/Thr235 (AT180) PubMed:22419736

Ectopic expression of AK1 in mouse cortical neurons increased immunoreactivity against phosphorylated tau at Ser396/404 (PHF-1), Ser202 (CP13) and Ser231/Thr235 (AT180) PubMed:22419736

Ectopic expression of AK1 in mouse cortical neurons increased immunoreactivity against phosphorylated tau at Ser396/404 (PHF-1), Ser202 (CP13) and Ser231/Thr235 (AT180) PubMed:22419736

The data suggest that the increased expres- sion of AK1 can enhance tau aggregation as well as tau phos- phorylation. PubMed:22419736

The data suggest that the increased expres- sion of AK1 can enhance tau aggregation as well as tau phos- phorylation. PubMed:22419736

In addition, we found that transient expression of AK1 (but not AK1 R132A mutant) markedly reduced the inhibitory phosphorylation of GSK3b at Ser9 (Fig. 4D and Supplemen- tary Material, S6A), indicating that AK1 may regulate GSK3b activity. PubMed:22419736

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. PubMed:22419736

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. PubMed:22419736

Co-expression of an AK1 transgene with tau in flies (gl-tau2.1/UAS-AK1) markedly enhanced tau-induced retinal degeneration,indicating that AK1 enhances tau toxicity in the fly retina. PubMed:22419736

These results indicate that AK1 exacerbates rough eye phenotype and tau hyperpho- sphorylation in a tauopathy model organism and that there is a close correlation between the exacerbated rough eye pheno- type and tau phosphorylation. PubMed:22419736

Co-expression of an AK1 transgene with tau in flies (gl-tau2.1/UAS-AK1) markedly enhanced tau-induced retinal degeneration,indicating that AK1 enhances tau toxicity in the fly retina. PubMed:22419736