کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4329877 | 1614239 | 2008 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of calpain and p25 of CDK5 pathway in ginsenoside Rb1's attenuation of β-amyloid peptide25-35-induced tau hyperphosphorylation in cortical neurons
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کلمات کلیدی
Aβcdk5NFTsGinsenoside Rb1p25p35Cyclin-dependent kinase 5 (Cdk5)β-Amyloid - β-آمیلوئیدβ-Amyloid (Aβ) - β-آمیلوئید (Aβ)Alzheimer's disease - بیماری آلزایمرTau - خود راMicrotubule - ریزلوله یا میکروتوبولcyclin-dependent kinase 5 - سیکلین وابسته به کیناز 5neurofibrillary tangles - مگس های نوروفیبریلیال
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Increasing evidence have shown that β-amyloid (Aβ) induced hyperphosphorylation of tau, which eventually resulted in the disruption of microtubule (MT) integrity. Cyclin-dependent kinase 5 (CDK5) and its activator p35 are required for neurite outgrowth. The cleavage of p35 to p25, mediated by calpain and calcium, caused CDK5 dislocation and subsequently p25/CDK5-induced tau hyperphosphorylation, which disrupted the cytoskeleton and resulted in neuronal death. In the present study we investigated the effects of ginsenoside Rb1 on fibrillar Aβ25-35-induced tau hyperphosphorylation in primary cultured cortical neurons and also the potential involvement of Ca2+-calpain-CDK5 signal pathway. The present study suggests that Ca2+, calpain, and p25 in CDK5 pathway may play important roles in Aβ25-35-induced tau hyperphosphorylation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1200, 20 March 2008, Pages 99-106
Journal: Brain Research - Volume 1200, 20 March 2008, Pages 99-106
نویسندگان
Xiaochun Chen, Tianwen Huang, Jing Zhang, Jinqiu Song, Limin Chen, Yuangui Zhu,