The tumor suppressor p53 serves as a “guardian of the genome” [1] and has been studied intensively for over 30 years. By responding to cellular stresses, such as DNA damage, hypoxia and cell-cycle aberrations, p53 is activated as a transcription factor. p53 can thus help to promote the repair and survival of damaged cells by inducing cell-cycle arrest, or it can promote the permanent removal of damaged cells by inducing programmed cell death or senescence

The tumor suppressor p53 serves as a “guardian of the genome” [1] and has been studied intensively for over 30 years. By responding to cellular stresses, such as DNA damage, hypoxia and cell-cycle aberrations, p53 is activated as a transcription factor. p53 can thus help to promote the repair and survival of damaged cells by inducing cell-cycle arrest, or it can promote the permanent removal of damaged cells by inducing programmed cell death or senescence