Circadian Proteins and Genotoxic Stress Response Biology Diagrams Taken together, these results suggest that IRE1α deficiency deregulates DDR signaling, thus affecting cell cycle progression, DNA repair and cell survival under genotoxic stress. Genotoxic stress
In mammalian cells, activation of stress-kinases by genotoxic stress can lead to cell-cycle delay at the G2-M transition, by intersecting with, and activating, the DNA-integrity checkpoints. It is apparent that stress kinases can be activated in an ATM-dependent manner in response to particular genotoxic stresses 52,53. Cell cycle checkpoints are critical components of the genotoxic stress response, acting as cellular "quality control" mechanisms. These checkpoints can temporarily halt cell cycle progression, providing time for DNA repair or, in cases of severe damage, initiating programmed cell death.
specific Measurement of γH2AX and Apoptosis After Genotoxic ... Biology Diagrams
To maintain the integrity of the genome, a cell challenged with genotoxic stress must sense the damage and respond to it by stalling cell cycle progression until the damage is repaired. If the damage is catastrophic, then pro-apoptotic mechanisms are activated, resulting in cell death. Genotoxic stress-mediated cell cycle activities for the decision of cellular fate Cell Cycle. 2011 Oct 1;10(19) :3239-48. (DDR) pathway. p53 induces the transcription of genes that negatively regulate progression of the cell cycle in response to DNA damage, and thus participates in maintaining genome stability. p53 and many other anti The purpose of this review is to discuss the known signal transduction pathways that regulate cell cycle progression and the mechanisms cells employ to insure DNA stability in the face of genotoxic stress. In particular, we focus on mammalian cell cycle checkpoint functions, their role in maintaining DNA stability during the cell cycle
For example, upon genotoxic stress, mitochondrial NAD + levels exhibit higher stability than nuclear and cytosolic NAD + pools, which is essential to cell viability 73. The presented method or slightly modified versions have been devised to study specific treatment responses and side effects of various anti-cancer treatments as used in clinical oncology. It enables a quantitative and longitudinal analysis of the DNA damage response after genotoxic stress, as induce …
