By Diane E. Spinelle
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Cycloheximide reduces the effects of anoxic insult in vivo and in vitro. Eur J Neurosci, 1992, 4, 758-765. M. G1/S cell cycle blockers and inhibitors of cyclin-dependent kinases suppress camptothecin-induced neuronal apoptosis. J Neurosci, 1997, 17, 1256-1270. C. A system for characterizing cellular and molecular events in programmed neuronal cell death. J Neurosci, 1993, 13, 36693680. , Charriaut-Marlangue, C. A model of transient unilateral focal ischemia with reperfusion in the P7 neonatal rat: morphological changes indicative of apoptosis.
2001), suggesting the importance of NHEJ pathway. , 2003; Bakkenist and Kastan, 2003). H2AX phosphorylation at serine 139 occurs at sites surrounding DSBs. ,2002). The ATM function is critical for many aspects of the DSB response (Shiloh, 2003). After DSB induction, ATM is rapidly activated by autophosphorylation (Bakkenist and Kastan, 2003). Active ATM then phosphorylates different substrates, involved in the DNA damage response. An important mediator of cell-cycle checkpoints and damage-induced apoptosis is the tumor suppressor protein p53, which is activated by ATM via various posttranslational modifications (Meek, 2004) or by phosphorylating Mdm2, a ubiquitin ligase of p53, thereby targeting p53 for degradation (Stommel and Wahl, 204).
A cell that has accumulated a large amount of DNA damage, or one that no longer effectively repairs damage, can enter one of three possible states:an irreversible state of dormancy, known as senescence, apoptosis, or mutagenesis and carcinogenesis (figure 1). The protection of genomic integrity, therefore, is a major challenge for living cells. To cope with the deadly consequences of DNA lesions, that interfere with essential DNA-dependent processes such as transcription and replication, cells are equipped with an efficient defense mechanism termed the DNA damage response.