Your browser doesn't support javascript.
loading
Activation of cell-cycle-associated proteins in neuronal death: a mandatory or dispensable path?
Copani, A; Uberti, D; Sortino, M A; Bruno, V; Nicoletti, F; Memo, M.
Afiliação
  • Copani A; Dept of Pharmaceutical Sciences, University of Catania, Viale A. Doria 6, 95125, Catania, Italy.
Trends Neurosci ; 24(1): 25-31, 2001 Jan.
Article em En | MEDLINE | ID: mdl-11163884
Cell-cycle-related proteins, such as cyclins or cyclin-dependent kinases, are re-expressed in neurons committed to death in response to a variety of insults, including excitotoxins, hypoxia and ischemia, loss of trophic support, or beta-amyloid peptide. In some of these conditions events that are typical of the mid-G1 phase, such as cyclin-dependent kinase 4/6 activation, are required for the induction of neuronal death. In other cases, the cycle must proceed further and recruit steps that are typical of the G1/S transition for death to occur. Finally, there are conditions in which cell-cycle proteins might be re-expressed, but do not contribute to neuronal death. We hypothesize that cell-cycle signaling becomes a mandatory component of neuronal demise when other mechanisms are not enough for neurons to reach the threshold for death. Under this scheme, the death threshold is set by the extent of DNA damage. Whenever the extent of DNA damage is below this threshold, a cell-cycle signaling becomes crucial for the induction of neuronal death through p53-dependent or -independent pathways.
Assuntos
Buscar no Google
Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Dano ao DNA / Peptídeos beta-Amiloides / Proteína Supressora de Tumor p53 / Apoptose / Proteínas de Ciclo Celular / Neurônios Tipo de estudo: Risk_factors_studies Limite: Animals / Humans Idioma: En Revista: Trends Neurosci Ano de publicação: 2001 Tipo de documento: Article
Buscar no Google
Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Dano ao DNA / Peptídeos beta-Amiloides / Proteína Supressora de Tumor p53 / Apoptose / Proteínas de Ciclo Celular / Neurônios Tipo de estudo: Risk_factors_studies Limite: Animals / Humans Idioma: En Revista: Trends Neurosci Ano de publicação: 2001 Tipo de documento: Article