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- W1981897425 endingPage "7256" @default.
- W1981897425 startingPage "7250" @default.
- W1981897425 abstract "A network of control pathways has been characterized that arrest growth or induce apoptosis in response to potentially tumorogenic events such as genotoxic stress or oncogene expression. Ablation, or functional disruption, of these pathways is frequently observed during multistep carcinogenesis. Analysis of those genes most commonly compromized in tumours has led to the identification of the transcription factor p53 and the E2F binding protein Retinoblastoma (Rb), as key regulators of these processes. This review discusses recent data, demonstrating that the Promyelocytic Leukemia (PML) protein can physically and functionally interact with both p53 and Rb, suggesting that PML may be a novel regulator of these pathways." @default.
- W1981897425 created "2016-06-24" @default.
- W1981897425 creator A5057101865 @default.
- W1981897425 creator A5090986303 @default.
- W1981897425 date "2001-10-29" @default.
- W1981897425 modified "2023-09-26" @default.
- W1981897425 title "PML interaction with p53 and its role in apoptosis and replicative senescence" @default.
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- W1981897425 doi "https://doi.org/10.1038/sj.onc.1204856" @default.
- W1981897425 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11704853" @default.
- W1981897425 hasPublicationYear "2001" @default.
- W1981897425 type Work @default.