کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8274177 | 1535097 | 2016 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Immunolocalization of Tom1 in relation to protein degradation systems in Alzheimer's disease
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کلمات کلیدی
PBSFBSAPPH&E - H & EAutophagy - اتوفاژیAlzheimer's disease - بیماری آلزایمرfetal bovine serum - سرم جنین گاوTollip - سفارشیDystrophic neurites - عصب های دیستروفیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریHematoxylin and Eosin - هماتوکسیلین و ائوزینamyloid precursor protein - پروتئین پیش ماده آمیلوئیUbiquitin - یوبیکویتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. Its pathological hallmarks are senile plaques (SPs), which contain extracellular deposits of amyloid β (Aβ) protein fibrils and dystrophic neurites (DNs), and neurofibrillary tangles (NFTs) containing hyperphosphorylated tau. Impairment of protein-degradation systems, including the ubiquitin-proteasome and the autophagy-lysosome systems, has been proposed as one of the causes of the accumulation of these aberrant proteins in AD brains. Tom1 (target of Myb1) was originally identified by the induction of its expression by the v-Myb oncogene and is a part of two major protein-degradation systems. The present study was conducted by immunohistochemical and immunofluorescent stainings to show that Tom1 was localized in DNs, perisomatic granules (PSGs), and NFTs in AD brains. Moreover, in DNs, Tom1 colocalized with ubiquitin, lysosomal proteins, and Tom1-related proteins (Tollip and myosin VI), which act in both protein-degradation systems via Tom1. These results indicate that Tom1 plays important roles in protein-degradation systems in AD pathogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the Neurological Sciences - Volume 365, 15 June 2016, Pages 101-107
Journal: Journal of the Neurological Sciences - Volume 365, 15 June 2016, Pages 101-107
نویسندگان
Kouki Makioka, Tsuneo Yamazaki, Masamitsu Takatama, Masaki Ikeda, Shigeo Murayama, Koichi Okamoto, Yoshio Ikeda,