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. 2000 May;2(3):208–225. doi: 10.1038/sj.neo.7900073

Figure 3.

Figure 3

The p53 response is triggered by many different stresses involving both DNA-damaging and non-DNA-damaging agents. These include ribonucleotide synthesis inhibitors resulting in perturbations of nucleotide pools [270], thymidine dinucleotides [271], media depletion [272], hypoxia [273], antioxidants [274,275], inhibition of ubiquitylation or the proteasome proteolysis pathway [53,107,108], DNA strand breaks [95], bulky DNA lesions [10,11], DNA topoisomerase inhibitors [11,276], blockage of RNA polymerase II [71–75], heat shock [273,277], cold shock [278], viral infection [217,279], pRb deregulation [216,280] and oncogene expression [214,215].