cellular
• following treatment with neocarzinostatin, which elicits double-stranded DNA breaks that mimic effects of ionizing radiation, mutant B cells display reduced Trp53 phosphorylation and increased cell viability relative to similarly-treated wild-type B cells
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• following exposure to ionizing radiation (2G or 5 G), mutant B cells show increased viability relative to similarly-treated wild-type B cells
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hematopoietic system
• mutant resting B cells show markedly reduced expression of DNA-PKcs and ATM, which are phosphoinositide-3-kinaserelated-kinases (PIKKs) shown to mediate the phosphorylation and apoptotic actions of Trp53
• in contrast, mutant MEFs show no alterations in levels of DNA-PKcs or ATM relative to wild-type MEFs
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immune system
• mutant resting B cells show markedly reduced expression of DNA-PKcs and ATM, which are phosphoinositide-3-kinaserelated-kinases (PIKKs) shown to mediate the phosphorylation and apoptotic actions of Trp53
• in contrast, mutant MEFs show no alterations in levels of DNA-PKcs or ATM relative to wild-type MEFs
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