IndraLab

Statements

TP53-K117R activates apoptotic process. 3 / 3
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"Analysis of cells derived from p53 K117R mice, carrying the acetylation site mutation that renders p53 defective for triggering apoptosis in cultured cells in vitro, confirmed that p53 K117R could not induce Puma or apoptosis in response to DNA damage, suggesting that acetylation at K117 is critical for p53 dependent apoptosis."
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"Further, p53 K117R; K161R; K162R is mutated at three p53 acetylation sites and can not induce cell cycle arrest, apoptosis, and senescence."
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"Moreover, to exclude the possibility that the mutant cells die with slower kinetics, we compared the levels of apoptosis induced by DNA damage in p53-wt, p53 K117R and K117R, p53 3KR/3KR and p53-null mice."
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