http://www.cnr.it/ontology/cnr/individuo/prodotto/ID17364
Ab(31-35) and Ab(25-35) fragments of amyloid beta-protein induce cellular death through apoptotic signals: Role of the redox state of methionine-35 (Articolo in rivista)
- Type
- Label
- Ab(31-35) and Ab(25-35) fragments of amyloid beta-protein induce cellular death through apoptotic signals: Role of the redox state of methionine-35 (Articolo in rivista) (literal)
- Anno
- 2005-01-01T00:00:00+01:00 (literal)
- Alternative label
Clementi M.E., Marini S., Coletta M., Orsini F., Giardina B., Misiti F. (2005)
Ab(31-35) and Ab(25-35) fragments of amyloid beta-protein induce cellular death through apoptotic signals: Role of the redox state of methionine-35
in FEBS letters (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Clementi M.E., Marini S., Coletta M., Orsini F., Giardina B., Misiti F. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- M. Elisabetta Clementi:CNR Institute \"Chimica del Riconoscimento Molecolare\"
Stefano Marini: Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Via di Tor Vergata, 135-00133 Rome, Italy
Massimo Coletta:Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Via di Tor Vergata, 135-00133 Rome, Italy
Federica Orsini: Institute of Biochemistry and Clinical Biochemistry and CNR Institute \"Chimica del Riconoscimento Molecolare\" Faculty of Medicine, Catholic University Largo F. Vito 1, 00168 Rome, Italy
Bruno Giardina: Institute of Biochemistry and Clinical Biochemistry and CNR Institute \"Chimica del Riconoscimento Molecolare\" Faculty of Medicine, Catholic University Largo F. Vito 1, 00168 Rome, Italy
Francesco Misiti: Department of \"Scienze Motorie e della Salute\", University of Cassino, V.le Bonomi, 03043 Cassino (FR), Italy (literal)
- Titolo
- Ab(31-35) and Ab(25-35) fragments of amyloid beta-protein induce cellular death through apoptotic signals: Role of the redox state of methionine-35 (literal)
- Abstract
- In order to clarify the basis of neuronal toxicity exerted by the shortest active peptides of amyloid beta-protein (A beta), the toxic effects of A beta(31-35) and A beta(25-35) peptides on isolated rat brain mitochondria were investigated. The results show that exposure of isolated rat brain mitochondria to A beta(31-35) and A beta(25-35) peptides determines: (i) release of cytochrome c; (ii) mitochondrial swelling and (iii) a significant reduction in mitochondrial oxygen consumption. In contrast, the amplitude of these events resulted attenuated in isolated brain mitochondria exposed to the A beta(31-35)Met35(OX) in which methionine-35 was oxidized to methionine sulfoxide. The AP peptide derivative with norleucine substituting Met-35, i.e., A beta(31-35)Nle-35, had not effect on any of the biochemical parameters tested. We have further characterized the action of A beta(31-35) and A beta(25-35) peptides on neuronal cells.
Taken together our result indicate that A beta(31-35) and A beta(25-35) peptides in non-aggregated form, i.e., predominantly monomeric, are strongly neurotoxic, having the ability to enter within the cells, determining mitochondrial damage with an evident trigger of apoptotic signals. Such a mechanism of toxicity seems to be dependent by the redox state of methionine-35. (literal)
- Prodotto di
- Autore CNR
Incoming links:
- Autore CNR di
- Prodotto
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi