PMID:14992722

Citation	de Stanchina, E, Querido, E, Narita, M, Davuluri, RV, Pandolfi, PP, Ferbeyre, G and Lowe, SW (2004) PML is a direct p53 target that modulates p53 effector functions. Mol. Cell 13:523-35
Abstract	The p53 tumor suppressor promotes cell cycle arrest or apoptosis in response to stress. Previous work suggests that the promyelocytic leukemia gene (PML) can act upstream of p53 to enhance transcription of p53 targets by recruiting p53 to nuclear bodies (NBs). We show that PML is itself a p53 target gene that also acts downstream of p53 to potentiate its antiproliferative effects. Hence, p53 is required for PML induction in response to oncogenes and DNA damaging chemotherapeutics. Furthermore, the PML gene contains p53 binding sites that confer p53 responsiveness to a heterologous reporter and can bind p53 in vitro and in vivo. Finally, cells lacking PML show a reduced propensity to undergo senescence or apoptosis in response to p53 activation, despite the induction of several p53 target genes. These results identify an additional element of PML regulation and establish PML as a mediator of p53 tumor suppressor functions.
Links	PubMed
Keywords	Animals; Apoptosis/genetics; Base Sequence; Binding Sites; Cell Aging/genetics; Cell Line; Cell Survival/genetics; Fibroblasts/cytology; Gene Expression Regulation, Neoplastic; Genes, Reporter; Genes, Tumor Suppressor; Genes, p53; Genes, ras; Humans; Leukemia, Promyelocytic, Acute/genetics; Mice; Mice, Knockout; Neoplasm Proteins/genetics; Nuclear Proteins; Promoter Regions, Genetic; Retroviridae/genetics; Signal Transduction; Transcription Factors/genetics; Tumor Suppressor Protein p53/metabolism; Tumor Suppressor Proteins
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Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
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