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In contrast, the transactivation-dead p5325,26,53,54 mutant cannot induce senescence or inhibit tumorigenesis, like p53 nullizygosity.
It is not clear why the S31G/S32G mutant cannot induce tetrasomy in monolayer but is capable of doing so in raft culture, but this differential ability is compatible with our previous hypothesis that the mechanisms of induction of basal and suprabasal tetrasomy are different (Southern et al, 2001).
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Interestingly, another p53 mutant, p53(25,26), cannot induce genes involved in acute DNA damage response while still maintaining the tumor suppressive function.
(Note: Seemingly in contrast, it was reported that mutant p53, which cannot induce arrest in response to DNA damage, can cause senescence [ 9].
In some cases the telomeres are lost and the resulting chromosome ends continually shorten as the mutants continue to divide because these unprotected ends cannot induce checkpoint-dependent cell cycle arrest in the absence of Mec1.
Here, we show that a Parkin RING domain mutant (C289G) fails to redistribute to damaged mitochondria and cannot induce mitophagy after treatment with the mitochondrial uncoupler carbonyl cyanide m-methylhydrazone, because of protein misfolding and aggregation.
Microarray analysis reveals that one mutant, p5325,26, is severely compromised for transactivation of most p53 target genes, and, moreover, p5325,26 cannot induce G1-arrest or apoptosis in response to acute DNA damage.
That is because, ultimately, the latter cannot induce the former.
RORγtM cannot induce genes encoding molecules critical for TH17 differentiation.
p53 cannot induce senescence without inducing arrest.
However, calcium channel blockers cannot induce catalepsy when administrated alone.
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