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- W4732561 abstract "Iron was shown to closely regulate the expression Alzheimer's Amyloid Precursor Protein (APP) gene at the level of message translation. Intracellular levels of APP holoprotein were shown to be modulated by a mechanism that is similar to the pathway by which iron controls the translation of the ferritin L- and H mRNAs by Iron-responsive Elements in their 5'untranslated regions (5'UTRs)[48]. More recently APP gene transcription was found to be responsive to copper deficit where the Menkes protein depleted fibroblasts of copper, an event that suppressed transcription of APP through metal regulatory and copper regulatory sequences upstream of the 5' cap site [1]. Genetic and biochemical evidence has also linked the biology of metals (Fe, Cu and Zn) to Alzheimer's disease. The genetic discovery that alleles in the hemochromatosis gene accelerate the onset of disease by five years [2] has certainly validated interest in the model wherein metals (iron) accelerate" @default.
- W4732561 created "2016-06-24" @default.
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- W4732561 date "2005-08-25" @default.
- W4732561 modified "2023-09-26" @default.
- W4732561 title "Amyloid Precursor Protein and Ferritin Translation: Implications for Metals and Alzheimer's Disease Therapeutics" @default.
- W4732561 doi "https://doi.org/10.1021/bk-2005-0903.ch013" @default.
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