کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3070119 1580714 2009 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Evidence of molecular links between PKR and mTOR signalling pathways in Aβ neurotoxicity: Role of p53, Redd1 and TSC2
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
پیش نمایش صفحه اول مقاله
Evidence of molecular links between PKR and mTOR signalling pathways in Aβ neurotoxicity: Role of p53, Redd1 and TSC2
چکیده انگلیسی

The control of translation is disturbed in Alzheimer's disease (AD). This study analysed the crosslink between the up regulation of double-stranded RNA-dependent-protein kinase (PKR) and the down regulation of mammalian target of rapamycin (mTOR) signalling pathways via p53, the protein Regulated in the Development and DNA damage response 1 (Redd1) and the tuberous sclerosis complex (TSC2) factors in two β-amyloid peptide (Aβ) neurotoxicity models. In SH-SY5Y cells, Aβ42 induced an increase of PT451-PKR and of the ratio p66/(p66 + p53) in nuclei and a physical interaction between these proteins. Redd1 gene levels increased and PT1462-TSC2 decreased. These disturbances were earlier in rat primary neurons with nuclear co-localization of Redd1 and PKR. The PKR gene silencing in SH-SY5Y cells prevented these alterations. p53, Redd1 and TSC2 could represent the molecular links between PKR and mTOR in Aβ neurotoxicity. PKR could be a critical target in a therapeutic program of AD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 36, Issue 1, October 2009, Pages 151–161
نویسندگان
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