p53 is required for radiation-induced apoptosis in mouse thymocytes

We have investigated the requirement for p53 during apoptosis in mouse thymocytes

Scott W. Lowe; Earlene M. Schmitt; Sallie W. Smith; Barbara A. Osborne; Tyler Jacks

2003

Scholarcy highlights

  • THE p53 tumour suppressor gene is the most widely mutated gene in human tumorigenesis1,2. p53 encodes a transcriptional activator whose targets may include genes that regulate genomic stability, the cellular response to DNA damage, and cell-cycle progression
  • Introduction of wild-type p53 into cell lines that have lost endogenous p53 function can cause growth arrest or induce a process of cell death known as apoptosis
  • Normal negative selection involves signalling through the T-cell receptor14, the induction of apoptosis by other stimuli is poorly understood
  • We have investigated the requirement for p53 during apoptosis in mouse thymocytes
  • We report here that immature thymocytes lacking p53 die normally when exposed to compounds that may mimic T-cell receptor engagement and to glucocorticoids but are resistant to the lethal effects of ionizing radiation. These results demonstrate that p53 is required for radiation-induced cell death in the thymus but is not necessary for all forms of apoptosis

Need more features? Save interactive summary cards to your Scholarcy Library.