This may increase the capacity of the cell to complete DNA repair. Inhibitors of poly(ADP-ribose) polymerase or deficiencies of the substrate, NAD, lead to retardation of the DNA repair process. When DNA strand breaks are extensive or when breaks fail to be repaired, the stimulus for ...
In the last fifteen years, rapid progress has been made in delineating the cellular response to DNA damage. The DNA damage response network is composed of a large number of proteins with different functions that detect and signal the presence of DNA damage in order to coordinate DNA repair with...
In the last fifteen years, rapid progress has been made in delineating the cellular response to DNA damage. The DNA damage response network is composed of a large number of proteins with different functions that detect and signal the presence of DNA damage in order to coordinate DNA repair with...
If a toxic stimulus is not removed, cells must adapt or they will die (Fulda et al., 2010). The cellular stress response (CSR) is an evolutionarily conserved mechanism of defense to an environmental stress that usually results in damage to lipids, proteins and DNA (Fulda et al., 2010;...
One such candidate for a central mediator of diverse E1A effects is the NK-κB activation pathway, which participates in the control of over 150 cellular target genes, including several involved in the response to apoptotic stimuli.44 We and others have reported that E1A represses stimulus-...
21However, the role of NF-κB in preventing apoptosis induced by chemotherapeutic agents is controversial. We and others have established that E1A-induced cellular sensitivity to apoptosis induced by TNF-superfamily members is mediated by inhibition of stimulus-induced, NF-κB-dependent transcription.6...
In the absence of a stress stimulus, TIP60 enhances TP53 stability by interfering with MDM2-mediated TP53 degradation, thus maintaining a basal pool of TP53 ready to respond to DNA damage. When DNA is damaged by a stress stimulus, TIP60 regulates K120 acetylation of TP53 and enhances TP53 ...
These reports suggest a proliferative function of p38 in contrast to the above mentioned role of p38 in stress response and cell cycle arrest. Some simple explanations for these discrepancies could be dependence on stimulus, cellular context or cell-type specificity. For example, p38 activation by ...
Necroptosis can also be ignited by pathogen recognition receptors, including Toll-like receptors, NOD-like receptors and retinoic acid-inducible gene I-like receptors, as well as in response to DNA damage, presumably by a poly(ADP-ribose) polymerase-1 (PARP1)-dependent signalling pathway. Although...
We conclude that analogous to oncogenic, oxidative and replicative stresses, bacterial intoxication represents another pathophysiological stimulus that induces premature senescence, an intrinsic cellular response that may mechanistically underlie the 'distended' morphology evoked by CDTs. Finally, the activation ...