http://www.cnr.it/ontology/cnr/individuo/prodotto/ID17698
Oxidation of methionine 35 reduces toxicity of the amyloid beta-peptide (1-42) in neuroblastoma cells (IMR-32) via enzyme methionine sulfoxide reductase A expression and function (Articolo in rivista)
- Type
- Label
- Oxidation of methionine 35 reduces toxicity of the amyloid beta-peptide (1-42) in neuroblastoma cells (IMR-32) via enzyme methionine sulfoxide reductase A expression and function (Articolo in rivista) (literal)
- Anno
- 2010-01-01T00:00:00+01:00 (literal)
- Alternative label
Misiti F., Clementi M.E., Giardina B. (2010)
Oxidation of methionine 35 reduces toxicity of the amyloid beta-peptide (1-42) in neuroblastoma cells (IMR-32) via enzyme methionine sulfoxide reductase A expression and function
in Neurochemistry international
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Misiti F., Clementi M.E., Giardina B. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- PubMed (literal)
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Misiti F: Department of Health and Motor Sciences, University of Cassino, V.S. Angelo, Polo didattico della Folcara, 03043 Cassino (FR), Italy
Clementi M.E: CNR Institute of \"Chimica del Riconoscimento Molecolare\", Largo F. Vito 1, 00168 Rome, Italy
Giardina B: CNR Institute and Institute of Biochemistry and Clinical Biochemistry, Catholic University School of Medicine, Largo F. Vito 1, 00168 Rome, Italy (literal)
- Titolo
- Oxidation of methionine 35 reduces toxicity of the amyloid beta-peptide (1-42) in neuroblastoma cells (IMR-32) via enzyme methionine sulfoxide reductase A expression and function (literal)
- Abstract
- The beta amyloid peptide (A beta), the major protein component of brain senile plaques in Alzheimer's disease, is known to be directly responsible for the production of free radicals that may lead to neurodegeneration. Our recent evidence suggest that the redox state of methionine residue in position 35 (Met-35) of A beta has the ability to deeply modify peptide's neurotoxic actions. Reversible oxidation of methionine in proteins involving the enzyme methionine sulfoxide reductase type A (MsrA) is postulated to serve a general antioxidant role and a decrease in MsrA has been implicated in Alzheimer's disease. In rat neuroblastoma cells (IMR-32), we used A beta(1-42), in which the Met-35 is present in the reduced state, with a modified peptide with oxidized Met-35 (A beta(1-42)Met35(ox)), as well as an A beta-derivative in which Met-35 is substituted with norleucine (A beta(1-42)Nle35) to investigate the relationship between Met-35 redox state, expression and function of MsrA and reactive oxygen species (ROS) generation. The obtained results shown that MsrA activity, as well as mRNA levels, increase in IMR-32 cells treated with A beta(1-42)Met35(ox), differently to that shown by the reduced derivative. The increase in MsrA function and expression was associated with a decline of ROS levels. None of these effects were observed when cells were exposed to A beta containing oxidized Met35 (A beta 1-42)Met35(ox). Taken together, the results of the present study indicate that the differential toxicity of A beta peptides containing reduced or oxidised Met-35 depends on the ability of the latter form to reduce ROS generation by enhancing MsrA gene expression and function and suggests the therapeutic potential of MsrA in Alzheimer's disease. (literal)
- Prodotto di
- Autore CNR
- Insieme di parole chiave
Incoming links:
- Autore CNR di
- Prodotto
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi
- Insieme di parole chiave di