In postmitotic sympathetic neurons, unlike most mitotic cells, death by apoptosis requires not only the release of cytochrome c from the mitochondria, but also an additional step to relieve X-linked inhibitor of apoptosis protein (XIAP)'s inhibition of caspases. Here, we examined the mechanism by which XIAP is inactivated following DNA damage and found that it is achieved by a mechanism completely different from that following apoptosis by nerve growth factor (NGF) deprivation. NGF deprivation relieves XIAP by selectively degrading it, whereas DNA damage overcomes XIAP via a p53-mediated induction of Apaf-1. Unlike wild-type neurons, p53-deficient neurons fail to overcome XIAP and remain resistant to cytochrome c after DNA damage. Restoring Apaf-1 induction in p53-deficient neurons is sufficient to overcome XIAP and sensitize cells to cytochrome c. Although a role for p53 in apoptosis upstream of cytochrome c release has been well established, this study uncovers an additional, essential role for p53 in regulating caspase activation downstream of mitochondria following DNA damage in neurons.
We study motivic amplitudes--objects which contain all of the
Essential mathematical content of scattering amplitudes in planar SYM theory in
A completely canonical way, free from the ambiguities inherent in any attempt
To choose particular functional representatives. We find that the cluster
We consider a non-autonomous dynamical system formed by coupling two
Piecewise-smooth systems in $\RR^2$ through a non-autonomous periodic
Perturbation. We study the dynamics around one of the heteroclinic orbits of
One of the piecewise-smooth systems. In the unperturbed case, the system
Small molecules are involved in metabolic pathways responsible for many biological activities. Therefore it is essential to study them to uncover the unknown biological function of highly complex living systems. It is a crucial step in modern drug discovery to correctly and effective...
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