Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/42259
Title: Inhibition of ataxia telangiectasia-p53-E2F-1 pathway in neurons as a target for the prevention of neuronal apoptosis
Author: Camins, A.
Verdaguer, E.
Folch, J.
Beas-Zárate, Carlos
Canudas, A.M.
Pallas, M.
Issue Date: 2007
Abstract: Over the last few decades, understanding of the mechanisms involved in the process of neuronal'cell death, has grown. Recent findings have established that DNA damage, and specifically ataxia telangiectasia mutated protein (ATM), is key to the castade of regulation of neuronal apoptosis. Another characteristic common to all neurodegenerative diseases is oxidative. stress. Likewise, a common feature in the brain of patients with neurodegenerative diseases such as Alzheimer's and Paskinson's diseases and other neurological disorders is the expression of proteins involved in cell-cycle control. In the process of re-entry in the cell cycle, an additional component, transcription factor E2F-1, also involved in the regulation of apoptosis, is expressed. Finally, in this complex puzzle, mitochondrial activation with the release of proteins and the activation of cystein proteases, specifically caspase-3, is prominent in the last step of neuronal apoptosis. This review focuses on the role of ATM activation and its re-entry into the cell cycle in neurons as a potential target for the prevention of neuronal apoptosis. We suggest the mechanisms by which ATM and E2F-1 orchestrate the apoptotic process. Among them, p53 could be a common point on this apoptotic route. Finally, we put forward drugs that are now being studied experimentally such as, p53 inhibitors, ATM inhibitors and cyclin-dependent kinase (CDKs) inhibitors, for the treatment of neurodegenerative diseases. © 2007 Bentham Science Publishers Ltd.
URI: http://www.scopus.com/inward/record.url?eid=2-s2.0-35348889576&partnerID=40&md5=9a1f1d9a13863dadadf5be7badf9e54a
http://hdl.handle.net/20.500.12104/42259
Appears in Collections:Producción científica UdeG

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