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. Author manuscript; available in PMC: 2014 Jan 30.
Published in final edited form as: Nat Rev Drug Discov. 2013 Jul;12(7):526–542. doi: 10.1038/nrd4003

Figure 4. The tissue-dependent role of p53 in the response of cells to radiation.

Figure 4

a | In unstressed cells, HDM2 ubiquitylates the tumour suppressor p53, leading to its degradation. Numerous cellular stresses increase the translation of TP53 mRNA and the phosphorylation of p53 protein, increasing its stability. p53 acts predominantly as a transcription factor that upregulates the expression of target genes to arrest cell growth or lead to cellular senescence and apoptosis, depending on the cellular context. Ribosomal protein |26 (RPL26) binds to TP53 mRNA and increases its translation. The p53 transcriptional targets GADD45 (growth arrest and DNA-damage-inducible protein 45) and p21 lead to cell cycle arrest, whereas BCL-2-associated X protein (BAX) and the BH3-only proteins PUMA (p53-upregulated modulator of apoptosis) and PMAIP1 (PMA-induced protein 1) can trigger apoptosis. b | The consequence Of p53 loss on the cellular radiation response varies depending on the type of tissue As a result, p53 inhibitors may be useful as both radiosensitizers and radioprotectors.