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E3 ligases and FKBP14 are potential drug targets for AD therapy

E3 ligases and FKBP14 are potential drug targets for AD therapy. Increasing the activity of non-canonical E3 ligases by drugs or gene therapy could prevent Tau aggregation. CHIP has been suggested to target phosphorylated Tau for ubiquitination and subsequent degradation;

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The proposed AD model that involves Tau phosphorylation, prion-like misfolded protein propagation, and the deregulation of UPS, HSP90, and FKBP co-chaperones

The proposed AD model that involves Tau phosphorylation, prion-like misfolded protein propagation, and the deregulation of UPS, HSP90, and FKBP co-chaperones. In AD, various physiological conditions are altered, including kinase over-expression or Aβ-induction increases in cellular kinase activities. As a

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Predicted interactions between Tau protein, FKBP and CHIP in AD

Predicted interactions between Tau protein, FKBP and CHIP in AD. FKBP12 catalyzes the hyperphosphorylated Tau assembly into PHF. The fate of HSP90-bound hyperphosphorylated Tau is determined by the binding of the HSP90 co-chaperone molecule. The binding of an FKBP51 co-chaperone

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The ubiquitin proteasome system and molecular chaperone deregulation in Alzheimer’s disease

The factors involved in the development of Alzheimer’s disease (AD) neuropathology. In the Tau-hypothesis, activation of cellular kinases may phosphorylate Tau, which subsequently causes Tau to lose its affinity to the microtubule system and thus forming aggregates. As an important

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