Combination of Abeta Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC
Combination of Abeta Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC(111 visite) Forestier A, Douki T, De Rosa V, Beal D, Rachidi W
Tipo di articolo: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 3.257, Impact factor a 5 anni: 3.213
Url: Non disponibile.
Parole chiave: Alzheimer, S Disease, Ddb2, Dna Damage, Dna Repair, Xpc, Neurodegenerative Disorders, Nucleotide Excision Repair, Oxidative Stress,
Affiliazioni:
*** IBB - CNR *** Laboratoire Lesions des Acides Nucleiques, Universite Joseph Fourier-Grenoble 1/CEA/Institut Nanoscience et Cryogenie/SCIB, UMR-E3, Grenoble, France. ann.forestier@gmail.com.
Riferimenti:
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Repair of oxidative DNA damage, particularly Base Excision Repair (BER), impairment is often associated with Alzheimer's disease pathology. Here, we aimed at investigating the complete Nucleotide Excision Repair (NER), a DNA repair pathway involved in the removal of bulky DNA adducts, status in an Alzheimer-like cell line. The level of DNA damage was quantified using mass spectrometry, NER gene expression was assessed by qPCR, and the NER protein activity was analysed through a modified version of the COMET assay. Interestingly, we found that in the presence of the Amyloid beta peptide (Abeta), NER factors were upregulated at the mRNA level and that NER capacities were also specifically increased following oxidative stress. Surprisingly, NER capacities were not differentially improved following a typical NER-triggering of ultraviolet C (UVC) stress. Oxidative stress generates a differential and specific DNA damage response in the presence of Abeta. We hypothesized that the release of NER components such as DNA damage binding protein 2 (DDB2) and Xeroderma Pigmentosum complementation group C protein (XPC) following oxidative stress might putatively involve their apoptotic role rather than DNA repair function.<br>
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240 Records (208 escludendo Abstract e Conferenze). Impact factor totale: 962.259 (850.533 escludendo Abstract e Conferenze). Impact factor a 5 anni totale: 1017.153 (888.056 escludendo Abstract e Conferenze).
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