کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9410761 | 1613317 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Abnormal intracellular trafficking of high affinity nerve growth factor receptor, Trk, in stable transfectants expressing presenilin 1 protein
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کلمات کلیدی
DMEMFBSPMSFNGFPS1Dulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccopresenilin 1 - Presenilin 1Autophosphorylation - اتوفسفورلاسیونDisorders of the nervous system - اختلالات سیستم عصبیAlzheimer's disease - بیماری آلزایمرDegenerative disease: Alzheimer's—miscellaneous - بیماری تخریب پذیر: آلزایمر- متفرقهTrk - تراکMutant - جهش یافتهfetal bovine serum - سرم جنین گاوnerve growth factor - فاکتور رشد عصبwild type - نوع وحشی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The pathogenesis of Alzheimer's disease (AD) is now thought to be tightly linked to Aβ deposition and oxidative stress, but it is still unknown how these factors result in neuronal dysfunction and cell death. Mutations of presenilin 1 (PS1) gene are the causative gene for early onset familial AD (FAD) due to the overproduction and deposition of pathogenic Aβ1-42 peptides. We report here the molecular influences of the overexpression of PS1 protein by stable transfection of PS1 cDNA into SH-SY5Y neuroblastoma cells on the function of high affinity nerve growth factor receptor, Trk, that is essential for neuronal survival and differentiation. We examined the sensitivity of these transfectants to oxidative stress and found that mutant (I143T) PS1-expressing clones showed the highest vulnerability to an oxidative stress inducer, hydrogen peroxide treatment compared with that of mock-transfected clones, whereas wild PS1-expressing cells were less vulnerable to the treatment than mutant PS1 transfectants. Because nerve growth factor (NGF) is known to protect neuronal cells from oxidative stress-induced cell death, we examined the NGF-Trk-mediated intracellular signaling pathway in these transfectants. In the wild and mutant PS1 cDNA-transfected cells, NGF did not elicit the autophosphorylation response of Trk, although their basal levels of tyrosine phosphorylation were higher than those of mock-transfected cells. Immunocytochemical and subcellular fractionation studies revealed that most of Trk proteins are abnormally located in the cytoplasm as well as in the nucleus in PS1-overexpressing clones irrespective of wild and mutant forms. These results strongly indicate that the expression level of PS1 protein has a cross talk with the Trk-dependent neuroprotective intracellular signaling pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Brain Research - Volume 137, Issues 1â2, 13 June 2005, Pages 70-76
Journal: Molecular Brain Research - Volume 137, Issues 1â2, 13 June 2005, Pages 70-76
نویسندگان
Tadanori Hamano, Tatsuro Mutoh, Takeshi Tabira, Wataru Araki, Masaru Kuriyama, Takateru Mihara, Shigeaki Yano, Hiroko Yamamoto,