We concluded that FKBP52 inhibits the promotion of microtubule assembly by Tau.
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.
In addition to its peptidyl–prolyl isomerase activity, FKBP52 serves as a molecular chaperone. This activity depends on its tetratricopeptide repeat domain (27) to which the molecular chaperone HSP90 and other proteins bind.
Thus, Tau and FKBP52 form a complex in rat brain. These findings indicate a direct interaction between FKBP52 and Tau. As shown in Fig. 3B, the amount of FKBP52 recruited by Tau depends on its phosphorylation state.In any case, these results underline the importance of Tau phosphorylation for its binding to FKBP52.
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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.