دورية أكاديمية
Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer's Disease.
| العنوان: | Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer's Disease. |
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| المؤلفون: | Bussiere, Renaud, Oulès, Bénédicte, Mary, Arnaud, Vaillant-Beuchot, Loan, Martin, Cécile, El Manaa, Wejdane, Vallée, Déborah, Duplan, Eric, Paterlini-Bréchot, Patrizia, Alves Da Costa, Cristine, Checler, Frédéric, Chami, Mounia |
| المصدر: | Cells, 8 (12) (2019) |
| بيانات النشر: | Multidisciplinary Digital Publishing Institute (MDPI) |
| سنة النشر: | 2019 |
| المجموعة: | University of Luxembourg: ORBilu - Open Repository and Bibliography |
| مصطلحات موضوعية: | Aged, 80 and over, Alzheimer Disease/genetics/metabolism/pathology, Amyloid Precursor Protein Secretases/metabolism, Amyloid beta-Peptides/metabolism, Amyloid beta-Protein Precursor/metabolism, Animals, Biomarkers, Brain/metabolism/pathology, Cell Line, Disease Models, Animal, Disease Susceptibility, Endoplasmic Reticulum Stress, Female, Gene Expression Regulation, Humans, Immunohistochemistry, Inflammation Mediators/metabolism, Isoenzymes, Male, Mice, Transgenic, Middle Aged, Models, Biological, Protein Aggregation, Pathological, Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics/metabolism, Signal Transduction |
| الوصف: | peer reviewed ; Dysregulation of the Endoplasmic Reticulum (ER) Ca(2+) homeostasis and subsequent ER stress activation occur in Alzheimer Disease (AD). We studied the contribution of the human truncated isoform of the sarco-endoplasmic reticulum Ca(2+) ATPase 1 (S1T) to AD. We examined S1T expression in human AD-affected brains and its functional consequences in cellular and transgenic mice AD models. S1T expression is increased in sporadic AD brains and correlates with amyloid β (Aβ) and ER stress chaperone protein levels. Increased S1T expression was also observed in human neuroblastoma cells expressing Swedish-mutated β-amyloid precursor protein (βAPP) or treated with Aβ oligomers. Lentiviral overexpression of S1T enhances in return the production of APP C-terminal fragments and Aβ through specific increases of β-secretase expression and activity, and triggers neuroinflammation. We describe a molecular interplay between S1T-dependent ER Ca(2+) leak, ER stress and βAPP-derived fragments that could contribute to AD setting and/or progression. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 2073-4409 |
| العلاقة: | urn:issn:2073-4409; https://orbilu.uni.lu/handle/10993/55927Test; info:hdl:10993/55927; https://orbilu.uni.lu/bitstream/10993/55927/1/Bussiere%20et%20al.%202019.pdfTest; info:pmid:31795302; wos:000506643500067 |
| DOI: | 10.3390/cells8121539 |
| الإتاحة: | https://doi.org/10.3390/cells8121539Test https://orbilu.uni.lu/handle/10993/55927Test https://orbilu.uni.lu/bitstream/10993/55927/1/Bussiere%20et%20al.%202019.pdfTest |
| حقوق: | open access ; http://purl.org/coar/access_right/c_abf2Test ; info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.DFED5B9 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 20734409 |
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| DOI: | 10.3390/cells8121539 |