The γ-secretase-generated intracellular domain of β-amyloid precursor protein binds Numb and inhibits Notch signaling

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• JNK-interacting protein-1 promotes transcription of Aβ protein precursor but not Aβ precursor-like proteins, mechanistically different than Fe65
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• BRI2 Inhibits Amyloid β-Peptide Precursor Protein Processing by Interfering with the Docking of Secretases to the Substrate
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• Numb Regulates Post-endocytic Trafficking and Degradation of Notch1
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• Profiling Identifies Precursor Suspects: Notch Family Again!
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• The intracellular threonine of amyloid precursor protein that is essential for docking of Pin1 is dispensable for developmental function.
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