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The results of our present study demonstrate that mitochondrial ROS generation in aging is stimulated by persistent activation of S6K1.
We have previously shown that learning-induced long-lasting post-burst AHP reduction is maintained by persistent activation of PKC and ERK [15], [16].
All animals were trained in a task that requires intact hippocampal function for learning, consolidation and recall [34] as well as hippocampal LTP maintenance by persistent activation of PKMζ for long-term memory storage [42], [55].
While it has been shown that olfactory-learning induced AHP reduction in piriform cortex neurons is maintained by persistent activation of both PKC and ERK [15], [16], it is still to be determined whether other key second messenger systems are also instrumental is such prolonged modulation of neuronal excitability.
Depletion of Gwl from Xenopus egg extracts impaired checkpoint recovery, as judged by persistent activation of checkpoint proteins and delayed reactivation of Cdk1 after removal of DNA damage.
Autoimmune diseases are caused by the breakdown of self-tolerance and are characterized by persistent activation of immune cells, leading to histopathological damage in the absence of an ongoing infection or other discernible cause [ 178].
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The defect in autophagy was accompanied by persistent activation via phosphorylation of Akt, mammalian target of rapamycin (mTOR) and of the autophagy-inhibiting pathways dependent on them, including the translation-initiation factor 4E-binding protein 1 and the ribosomal protein S6, and downregulation of the autophagy-inducing genes LC3, Atg12, Gabarapl1 and Bnip3.
Late LTP is induced by changes in gene expression and protein synthesis brought about by the persistent activation of protein kinases activated during E-LTP, such as MAPK.
The ROS-induced apoptosis is commonly mediated by the persistent activation of JNK and p38 MAPK pathways (Junttila et al, 2008).
It is quite possible, therefore, that axonal TRPV1, just like peripheral terminal TRPV1, may also become sensitized by the persistent activation of the PKRs due to the presence of PROK2.
Surprisingly, these cells escaping the G2/M DNA damage checkpoint are not driven to apoptosis but are accumulated in the next G0/G1 phase, suggesting that apoptosis is triggered by a persistent activation of the DNA damage response in G2/M cells.
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Justyna Jupowicz-Kozak
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