Genome instability contributes to cancer development, while radiation and chemotherapy routinely rely on inflicting genotoxic stress to trigger apoptotic demise of cancer cells. DNA damage response (DDR) pathways that are mediated through the tumor suppressor p53 play an important role in the cell intrinsic responses to genome instability, including a transient cell cycle arrest, senescence and apoptosis.
Also non-cell autonomous interactions of the p53 network with the innate immune system and the systemic adjustments during the aging process comprise important aspects of p53-mediated tumor suppression. The network of p53 target genes thus functions as an important regulator of cancer prevention, tumor therapy responses and also the physiological adjustments during aging.
To gain a better understanding of the mechanisms of the differential outcomes of p53 activity, we aim to investigate by in vitro and in vivo live imaging of key effectors of the p53-mediated DDR.
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Institute for Genome Stability in Ageing and Disease | CECAD Research Center
CMMC - PI - A 10show more…