DNA-DAMAGE CAN INDUCE APOPTOSIS IN PROLIFERATING LYMPHOID-CELLS VIA P53-INDEPENDENT MECHANISMS INHIBITABLE BY BCL-2
- Author(s)
- Strasser, A; Harris, AW; Jacks, T; Cory, S;
- Details
- Publication Year 1994-10-21,Volume 79,Issue #2,Page 329-339
- Journal Title
- CELL
- Publication Type
- Journal Article
- Abstract
- The roles of p53 as an inducer and Bcl-2 as an inhibitor of apoptotic death were explored in lymphoid cells. Lymphocytes from p53(-/-) mice were radioresistant, but unexpectedly, cycling T lymphoma cells and mitogenically activated T lymphocytes from these animals underwent apoptosis after irradiation or genotoxic drug treatment. Hence, p53 is not the only mediator of apoptosis provoked by DNA damage. Irradiated p53(-/-) lymphoblasts expressing Bcl-2 were subject to growth arrest but resisted apoptosis. Their accumulation in G1 as well as G2 is suggestive of a p53-independent DNA-damage G1 checkpoint. Since Bcl-2 increased the clonogenic survival of the irradiated cells, expression of survival genes may pose a greater impediment to genotoxic cancer therapy than loss of p53.
- Publisher
- CELL PRESS
- Keywords
- WILD-TYPE P53; MYELOID-LEUKEMIA CELLS; DEATH GENE CED-3; CYCLE CONTROL; ERYTHROLEUKEMIA-CELLS; MICE DEFICIENT; STRAND BREAKS; MUTANT P53; PRE-B; PROTEIN
- Publisher's Version
- https://doi.org/10.1016/0092-8674(94)90201-1
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1994-10-21 12:00:00