Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/65629
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dc.contributor.authorCamins, A.
dc.contributor.authorVerdaguer, E.
dc.contributor.authorFolch, J.
dc.contributor.authorBeas-Zárate, Carlos
dc.contributor.authorCanudas, A.M.
dc.contributor.authorPallas, M.
dc.date.accessioned2015-11-19T18:50:32Z-
dc.date.available2015-11-19T18:50:32Z-
dc.date.issued2007
dc.identifier.urihttp://hdl.handle.net/20.500.12104/65629-
dc.description.abstractOver 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.
dc.titleInhibition of ataxia telangiectasia-p53-E2F-1 pathway in neurons as a target for the prevention of neuronal apoptosis
dc.typeReview
dc.identifier.doi10.2174/138920007782109814
dc.relation.ispartofjournalCurrent Drug Metabolism
dc.relation.ispartofvolume8
dc.relation.ispartofissue7
dc.relation.ispartofpage709
dc.relation.ispartofpage715
dc.subject.keywordApoptosis; Cyclin dependent kinases; E2F-1; Neuron
dc.contributor.affiliationCamins, A., Unitat de Farmacologia i Farmacognòsia, Facultad de Farmàcia, Universitat de Barcelona, E-08028 Barcelona, Spain, Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, E-08028 Barcelona, Spain; Verdaguer, E., Departament de Farmacologia i Toxicologia, IIBB-CSIC, IDIBAPS, Rossello 161, 08036 Barcelona, Spain; Folch, J., Unitat de Bioquimica, Facultad de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, C./ St. Llorenç 21, 43201 Reus Tarragona, Spain; Beas-Zarate, C., Laboratorio de Néurobiología Celular y Molecular, División de Neurociencias, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, Laboratorio de Desarrollo y Regeneración Neural, Instituto de Neurobiología, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Canudas, A.M., Unitat de Farmacologia i Farmacognòsia, Facultad de Farmàcia, Universitat de Barcelona, E-08028 Barcelona, Spain, Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, E-08028 Barcelona, Spain; Pallàs, M., Unitat de Farmacologia i Farmacognòsia, Facultad de Farmàcia, Universitat de Barcelona, E-08028 Barcelona, Spain, Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, E-08028 Barcelona, Spain
dc.contributor.affiliationBeas-Zárate, Carlos., Universidad de Guadalajara. Centro Universitario de Ciencias Biológicas y Agropecuarias
dc.relation.isReferencedByScopus
dc.relation.isReferencedByWOS
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-35348889576&partnerID=40&md5=9a1f1d9a13863dadadf5be7badf9e54a
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