Pages that link to "Q40108106"

The following pages link to Gleevec increases levels of the amyloid precursor protein intracellular domain and of the amyloid-beta degrading enzyme neprilysin (Q40108106):

Displaying 27 items.

• The Alzheimer's amyloid-degrading peptidase, neprilysin: can we control it? (Q21296650) (← links)
• Peripheral Delivery of a CNS Targeted, Metalo-Protease Reduces Aβ Toxicity in a Mouse Model of Alzheimer's Disease (Q27437619) (← links)
• The Amyloid Precursor Protein Has a Flexible Transmembrane Domain and Binds Cholesterol (Q27679405) (← links)
• Co-localization of the amyloid precursor protein and Notch intracellular domains in nuclear transcription factories (Q30494474) (← links)
• Association of differential gene expression with imatinib mesylate and omacetaxine mepesuccinate toxicity in lymphoblastoid cell lines (Q34392064) (← links)
• Potential role of Notch signalling in CD34 chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL (Q35596540) (← links)
• The role of γ-secretase activating protein (GSAP) and imatinib in the regulation of γ-secretase activity and amyloid-β generation (Q36562023) (← links)
• Nicastrin is required for APP but not Notch processing, while Aph-1 is dispensable for processing of both APP and Notch (Q37056420) (← links)
• Polyhydroxycurcuminoids but not curcumin upregulate neprilysin and can be applied to the prevention of Alzheimer's disease. (Q37089706) (← links)
• Mechanisms of Amyloid-β Peptide Clearance: Potential Therapeutic Targets for Alzheimer's Disease (Q37224550) (← links)
• Neprilysin and Aβ Clearance: Impact of the APP Intracellular Domain in NEP Regulation and Implications in Alzheimer's Disease (Q37408544) (← links)
• Original Research: Featured Article: Imatinib mesylate (Gleevec) inhibits Notch and c-Myc signaling: Five-day treatment permanently rescues mammary development (Q37551137) (← links)
• Troubleshooting methods for APP processing in vitro (Q37691942) (← links)
• Are amyloid‐degrading enzymes viable therapeutic targets in Alzheimer’s disease? (Q37961852) (← links)
• The physiology of the β-amyloid precursor protein intracellular domain AICD. (Q37961985) (← links)
• The amyloid precursor protein: a biochemical enigma in brain development, function and disease (Q38107684) (← links)
• Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer's disease (Q38256360) (← links)
• BRI2 Protein Regulates β-Amyloid Degradation by Increasing Levels of Secreted Insulin-degrading Enzyme (IDE) (Q38795575) (← links)
• New Insights into Epigenetic and Pharmacological Regulation of Amyloid-Degrading Enzymes (Q38834930) (← links)
• Do Cancer Drugs Counteract Neurodegeneration? Repurposing for Alzheimer's Disease. (Q39005365) (← links)
• Surfaceome profiling reveals regulators of neural stem cell function (Q39097529) (← links)
• An alternative metabolic pathway of amyloid precursor protein C‐terminal fragments via cathepsin B in a human neuroglioma model (Q39508787) (← links)
• Neprilysin gene expression requires binding of the amyloid precursor protein intracellular domain to its promoter: implications for Alzheimer disease (Q39908636) (← links)
• Hypoxia Affects Neprilysin Expression Through Caspase Activation and an APP Intracellular Domain-dependent Mechanism. (Q40263247) (← links)
• ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease (Q42077676) (← links)
• Quantitative Measurement of γ-Secretase-mediated Amyloid Precursor Protein and Notch Cleavage in Cell-based Luciferase Reporter Assay Platforms (Q50010638) (← links)
• The Aβ-clearance protein transthyretin, like neprilysin, is epigenetically regulated by the amyloid precursor protein intracellular domain. (Q52840245) (← links)