By Diane E. Spinelle
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1991). AP endonuclease 1 (Ape1) cleaves the DNA backbone, which permits incorporation of a correct nucleotide by DNA 26 Inna I. Kruman and Elena I. , 1998). , 1998). Single-Strand Break Repair SSBs arise primarily from attack by ROS, whereas indirect SSBs are mainly normal intermediates of DNA BER, as a result of AP endonuclease activity and before they are "handed" to the next enzyme in the BER process, in a molecular relay. In addition to being the most common ‘endogenous’ lesion (thousands per cell per day) SSBs are also the most common lesions induced by exogenous genotoxins such as ionizing radiation, and alkylating agents (Caldecott, 2004).
Transient hypoxia may lead to neuronal proliferation in the developing mammalian brain: from apoptosis to cell cycle completion. Neuroscience, 1999a, 91, 221-231. L. CPP32/CASPASE-3-like proteases in hypoxia-induced apoptosis in developing brain neurons, Mol. Brain Res, 1999b 71, 225237. L. Involvement of caspase-1 proteases in hypoxic brain injury. Effects of their inhibitors in developing neurons, Neuroscience, 2000, 95, 1157-1165. L. Sequential expression patterns of apoptosis- and cell cycle-related proteins in neuronal response to severe or mild transient hypoxia.
In addition, E2F functions in apoptosis following DNA damage and regulates expression of pro-apoptotic genes including apaf-1 and several caspases (DeGregori, 2002). ATM and ATR are thought to be involved in the transmission of signals from stalled replication forks through a multitude of signaling cascades. , 1999). Thus, DNA-damage may induce apoptosis through E2F-1. e. not complexed with retinoblastoma protein Rb (pRb) and thus most active during this phase of the cell-cycle (Harbour and Dean, 2000).