Abstract
Deficiency of p63, a p53-related protein, causes severe defects in epithelial morphogenesis. Studies of p63-compromised mouse models reveal that p63 deficiency induces cellular senescence both in cultured cells and in vivo, through regulation p19(Arf)/p53 and p16(Ink4a)/Rb pathways. An extensive tumor study of p63-compromised mice demonstrated that p63 deficiency does not predispose to, but rather protects from, tumor development. These findings further implicate p63 as a negative regulator of the tumor suppressive mechanism of cellular senescence.
MeSH terms
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Animals
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Cellular Senescence / genetics
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Cellular Senescence / physiology*
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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DNA-Binding Proteins / physiology*
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Humans
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Models, Biological
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Neoplasms / genetics
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Neoplasms / pathology
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Neoplasms / physiopathology*
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Trans-Activators / genetics
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Trans-Activators / metabolism
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Trans-Activators / physiology*
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Transcription Factors
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism
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Tumor Suppressor Proteins / physiology*
Substances
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DNA-Binding Proteins
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TP63 protein, human
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Trans-Activators
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Transcription Factors
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Tumor Suppressor Proteins