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The nature of the cell cycle in neurons: Focus on a "non-canonical" pathway of DNA replication causally related to death

被引：45
作者：
Copani, Agata
Caraci, Filippo
Hoozemans, Jeroen J. M.
Calafiore, Marco
Sortino, Maria Angela
Nicoletti, Ferdinando
机构：
[1] Univ Roma La Sapienza, Dept Human Physiol & Pharmacol, I-00185 Rome, Italy
[2] Univ Catania, Dept Pharmaceut Sci, I-95124 Catania, Italy
[3] CNR, IBB, Catania, Italy
[4] Univ Amsterdam, Acad Med Ctr, Dept Neuropathol, NL-1012 WX Amsterdam, Netherlands
[5] Univ Catania, Dept Clin & Expt Pharmacol, I-95124 Catania, Italy
[6] INM Neuromed, Pozzilli, Italy
[7] Univ Catania, gPHD Program Neuropharmacol, I-95124 Catania, Italy
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2007年 / 1772卷 / 04期
关键词：
Alzheimer's disease; beta-amyloid; DNA polymerase-beta; APE-1; cell cycle; DNA replication; apoptosis; DEPENDENT KINASE INHIBITORS; AMYOTROPHIC-LATERAL-SCLEROSIS; ALZHEIMERS-DISEASE; POLYMERASE-BETA; TEMPORAL CORTEX; ACTIVATION; EXPRESSION; APOPTOSIS; EVENTS; INVOLVEMENT;
D O I：
10.1016/j.bbadis.2006.10.016
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The mechanism whereby a reactivation of cell cycle in neurons causes cell death is beginning to be identified. In cellular models of Alzheimer's disease, activation of a non-canonical pathway of DNA replication contributes to neuronal death. This pathway involves the repair enzyme DNA polymerase-beta, which is highly expressed in neurons of the Alzheimer's brain at early stages of the disease. Loading of DNA polymerase-beta into the replication forks generates a death signal, which involves the turner suppressor p53. The increasing knowledge of the main actors of the unscheduled DNA replication in neurons will pave the way for novel therapeutic interventions in Alzheimer's disease and other neurodegenerative disorders. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码：409 / 412
页数：4
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