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. 2014 Oct 17;106(11):dju329. doi: 10.1093/jnci/dju329

Figure 4.

Figure 4.

DNA damage secondary to radiotherapy induces the activation of DNA-protein kinases (DNA-PK), ataxia telangiectasia mutated, and ataxia telangiectasia and Rad3-related proteins, which subsequently induce p53 via phosphorylation of various substrates. In sarcomas overexpressing murine double minute 2 homolog (MDM2), p53 is targeted by MDM2 for ubiquitination and degradation, thereby inhibiting p53’s ability to induce cell cycle arrest, apoptosis, and senescence. ATM = ataxia telangiectasia mutated; ATR = ataxia telangiectasia and Rad3-related proteins; RT = radiotherapy.