Note for: Disruption of ATM in p53-null cells causes multiple functional abnormalities in cellular response to ionizing radiation
00609_Disruption of ATM in p53-null cells causes multiple functional abnormalities in cellular response to ionizing radiation (doi: 10.1038/sj.onc.1203172) Points - belong to phosphatidylinositol-3 kinase family - Using DT40 to study the function of ATM DT40 does not express p53 - ATM(-/-) - retard in growth, defect in G2/M checkpoint, radio-resistant DNA synthesis - sensitive to ionizing radiation - higher in spontaneous chromosomal aberrations - higher in radiation-induced chromosomal aberrations - slight reduction in targeted integration frequency - all above properties indicated p53-independent ATM functions p53 is the key player for 1. cell cycle checkpoint control 2. apoptosis 3. DNA repair (work through the downstream of ATM phosphorylation -- p53 is the substrate of ATM) DT40 lacks p53 expression, but ATM(-/-)DT40 - defect in 1. cell cycle checkpoint control 2. DNA repair (this means there is another p53 independent mechanisms co...