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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 4

act(p(HGNCGENEFAMILY:Proteasome)) increases deg(p(RGD:Mapt)) View Subject | View Object

For example, in the study where rat brain extract was incubated with Mg2+ and ATP, there was an overall decrease in tau due to proteasomal activity; however tau phosphorylated at the PHF1 and Tau-1 epitopes seemed to be preferentially degraded as they were non-detectable within 3 h (73). The preferential degradation of specific phospho-forms of tau by a particular pathway has been reported in other studies as well. PubMed:24027553

p(RGD:Fkbp4) decreases act(p(RGD:Mapt)) View Subject | View Object

We concluded that FKBP52 inhibits the promotion of microtubule assembly by Tau. PubMed:20133804

Out-Edges 16

act(p(RGD:Mapt)) increases bp(GO:"microtubule polymerization") View Subject | View Object

We concluded that FKBP52 inhibits the promotion of microtubule assembly by Tau. PubMed:20133804

act(p(RGD:Mapt)) increases bp(GO:"neuron projection development") View Subject | View Object

Because one role of Tau is to stimulate neurite outgrowth (12), we investigated the consequence of FKBP52 overexpression on neurite length in both PC12 and H7C2 cells. The inhibition of neurite outgrowth resulting from FKBP52 overexpression is in agreement with our previous report showing that the loss of FKBP52 in PC12 cells results in the formation of neurite extensions (9). The FKBP52 effect on neurite length could be explained by the binding of Tau to FKBP52, removing Tau from microtubules. PubMed:20133804

Annotations
Experimental Factor Ontology (EFO)
PC12

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