By Diane E. Spinelle
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This reflects the intimate relationship between ATM, cell cycle activation, and DNA repair in postmitotic neurons, and further suggests that cell cycle reentry is a requisite component of the response to DNA damage essential for the execution of both apoptosis and DNA repair in neurons. , 2002). , 1999). , 1996). , 2000). Oxidative stress and oxidative DNA damage induce up-regulation of OGG1 activity associated with this type of DNA damage. In support of these observations, we found up-regulated levels of UNG mRNA in brains of cystathionine-β-synthase-knockout (CBS) mice compared to wild-type mice.
Apoptotic features in ischemia, epilepsy and gp 120 toxicity. Trends in Neurosci, 1996, 19, 109-114. , Ben-Ari, Y. DNA damage and DNA damage-inducible protein Gadd45 following ischemia in the P7 neonatal rat. Dev Brain Res, 1999, 116, 133-140. L. Sequential activation of activator protein-1-related transcription factors and JNK protein kinases may contribute to apoptotic death induced by transient hypoxia in developing brain neurons. Mol Brain Res, 1998, 63, 105-120. , Vert, P. Neonatal hypoxia triggers transient apoptosis followed by neurogenesis in the rat CA1 hippocampus.
First, the DNA lesions are detected by sensor proteins. Damage to DNA modifies the spatial configuration of the helix and these modifications can be detected by the cell. Transducers initiate a signal transduction cascade that amplifies the signal and conveys the damage signal 24 Inna I. Kruman and Elena I. Schwartz to downstream effectors. When damage is localized, specific DNA repair molecules, which are part of the whole DNA repair machinery, are recruited and bind at the site of damage, inducing other molecules to bind and form a complex that facilitates the actual DNA repair mechanism.