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• W1623897355 endingPage "951" @default.
• W1623897355 startingPage "941" @default.
• W1623897355 abstract "The study of the adaptive response, i.e. a reduced effect from a higher challenging dose of a stressor when a smaller inducing dose had been applied a few hours earlier, has opened many new vistas into the mechanisms by which cells can adapt to hazardous environments. Although the entire chain from the initial event, supposedly the presence of DNA damage, to the end effect, presumably improved DNA repair, has not been fully elucidated, many individual links have been postulated. Initial elements--following the still unknown signal for the presence of radiation damage--are various kinases (protein kinase C and stress-activated protein kinases), which, in turn, induce early response genes whose products initiate a cascade of protein-DNA interactions that regulate gene transcription and ultimately result in specific biological responses. These responses include the activation of later genes that can promote production of growth factors and cytokines, trigger DNA repair, and regulate progress through the cell cycle. Indeed, there appears to be a relation between the induction of the adaptive response and the effects of radiation and cytostatic agents on the cell cycle, although these effects, especially the G1 delay, occur at much higher doses than the adaptive response, and one may not indiscriminately extrapolate mechanisms responsible for cell cycle changes observed at high doses, e.g. for radiation in the order of grays, to those involved in the adaptive responses at much lower doses, i.e. some tens of milligrays." @default.
• W1623897355 created "2016-06-24" @default.
• W1623897355 creator A5011600377 @default.
• W1623897355 creator A5023004617 @default.
• W1623897355 date "1998-04-01" @default.
• W1623897355 modified "2023-09-25" @default.
• W1623897355 title "Adaptive Response to DNA-Damaging Agents" @default.
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• W1623897355 doi "https://doi.org/10.1016/s0006-2952(97)00448-6" @default.
• W1623897355 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9605418" @default.
• W1623897355 hasPublicationYear "1998" @default.
• W1623897355 type Work @default.

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