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- W2186102610 abstract "P53 homolog p63 was shown to play a role in premature ageing phenotype found in mouse models through regulation of the replicative senescence. We previously showed that the forced ÎNp63α expression decreased the SIRT1 protein levels, and induced the replicative senescence of human keratinocytes, while the ectopic SIRT1 expression decreased the senescence. Using the ÎNp63α overexpressing and p63-/+ heterozygous mice, we found that ÎNp63α induced the mTERT promoter activation through the down regulation of the SIRT1 protein levels, inactivation of p53 deacetylation, decrease of the p53/Sp1 protein-protein interaction, and the overall induction of mTERT transcription regulation. In the same time, by a forming of protein-protein complexes with the ABBP1, ÎNp63α induced the mTERT RNA splicing leading to an increasing expression of spliced mTERT isoforms playing a role of dominant-negative inhibitors of mTERT activity and therefore decreasing the levels of TERT activity in mouse epidermal keratinocytes. The overall effect of the ÎNp63α overexpression resulted in decrease in telomerase activity and increase in replicative senescence observed in mouse keratinocytes. This dual molecular mechanism of telomerase regulation might underline the previously shown effect of ÎNp63α on premature ageing phenotype." @default.
- W2186102610 created "2016-06-24" @default.
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- W2186102610 date "2008-12-09" @default.
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- W2186102610 title "Dual regulation of TERT activity through transcription and splicing by ΔNP63α" @default.
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- W2186102610 doi "https://doi.org/10.18632/aging.100003" @default.
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