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Christophorou, M.A., Ringshausen, I., Finch, A.J., Swigart, L.B., Evan, G.I., The pathological response to DNA damage does not contribute to p53-mediated tumour suppression. Nature 443 (2006), 214–217.
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Brady, C.A., Jiang, D., Mello, S.S., Johnson, T.M., Jarvis, L.A., Kozak, M.M., Broz, D.K., Basak, S., Park, E.J., McLaughlin, M.E., et al. Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression. Cell 145 (2011), 571–583.
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Li, T., Kon, N., Jiang, L., Tan, M., Ludwig, T., Zhao, Y., Baer, R., Gu, W., Tumor suppression in the absence of p53-mediated cell-cycle arrest, apoptosis, and senescence. Cell 149 (2012), 1269–1283.
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Valente Liz, J., Gray Daniel, H.D., Michalak Ewa, M., Pinon-Hofbauer, J., Egle, A., Scott Clare, L., Janic, A., Strasser, A., p53 efficiently suppresses tumor development in the complete absence of its cell-cycle inhibitory and proapoptotic effectors p21, Puma, and Noxa. Cell Rep 3 (2013), 1339–1345.
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Hemann, M.T., Zilfou, J.T., Zhao, Z., Burgess, D.J., Hannon, G.J., Lowe, S.W., Suppression of tumorigenesis by the p53 target PUMA. Proc Natl Acad Sci U S A 101 (2004), 9333–9338.
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Valente, L.J., Grabow, S., Vandenberg, C.J., Strasser, A., Janic, A., Combined loss of PUMA and p21 accelerates c-MYC-driven lymphoma development considerably less than loss of one allele of p53. Oncogene 35 (2016), 3866–3871.
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Sengupta, S., Harris, C.C., p53: traffic cop at the crossroads of DNA repair and recombination. Nat Rev Mol Cell Biol 6 (2005), 44–55.
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Ganem Neil, J., Cornils, H., Chiu, S.-Y., O'Rourke Kevin, P., Arnaud, J., Yimlamai, D., Théry, M., Camargo Fernando, D., Pellman, D., Cytokinesis failure triggers hippo tumor suppressor pathway activation. Cell 158 (2014), 833–848.
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14
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84994464146
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p53 activity results in DNA replication fork processivity
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This paper reports that p53 activation can enhance replication fork progression, a mechanism through which p53 can promote genomic stability.
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Klusmann, I., Rodewald, S., Müller, L., Friedrich, M., Wienken, M., Li, Y., Schulz-Heddergott, R., Dobbelstein, M., p53 activity results in DNA replication fork processivity. Cell Rep 17 (2016), 1845–1857 This paper reports that p53 activation can enhance replication fork progression, a mechanism through which p53 can promote genomic stability.
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Klusmann, I.1
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15
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p53 maintains genomic stability by preventing interference between transcription and replication
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This paper describes a new function of p53 — the coordination between transcription and replication — which is important for promoting normal replication fork progression.
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Yeo, C.Q., Alexander, I., Lin, Z., Lim, S., Aning, O.A., Kumar, R., Sangthongpitag, K., Pendharkar, V., Ho, V.H., Cheok, C.F., p53 maintains genomic stability by preventing interference between transcription and replication. Cell Rep 15 (2016), 132–146 This paper describes a new function of p53 — the coordination between transcription and replication — which is important for promoting normal replication fork progression.
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Yeo, C.Q.1
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16
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p53 genes function to restrain mobile elements
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Using Drosophila, zebrafish, and human cancer cells, Wylie et al. show that p53 can restrict retrotransposon activity, thereby preserving genome integrity and suggesting a mechanism for tumor suppression.
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Wylie, A., Jones, A.E., D'Brot, A., Lu, W.-J., Kurtz, P., Moran, J.V., Rakheja, D., Chen, K.S., Hammer, R.E., Comerford, S.A., et al. p53 genes function to restrain mobile elements. Genes Dev 30 (2015), 64–77 Using Drosophila, zebrafish, and human cancer cells, Wylie et al. show that p53 can restrict retrotransposon activity, thereby preserving genome integrity and suggesting a mechanism for tumor suppression.
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Wylie, A.1
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17
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P53 and the defenses against genome instability caused by transposons and repetitive elements
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Levine, A.J., Ting, D.T., Greenbaum, B.D., P53 and the defenses against genome instability caused by transposons and repetitive elements. Bioessays 38 (2016), 508–513.
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Levine, A.J.1
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The evolution of thymic lymphomas in p53 knockout mice
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Dudgeon, C., Chan, C., Kang, W., Sun, Y., Emerson, R., Robins, H., Levine, A.J., The evolution of thymic lymphomas in p53 knockout mice. Genes Dev 28 (2014), 2613–2620.
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Dudgeon, C.1
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19
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p53 is essential for DNA methylation homeostasis in naïve embryonic stem cells, and its loss promotes clonal heterogeneity
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Tovy, A., Spiro, A., McCarthy, R., Shipony, Z., Aylon, Y., Alton, K., Ainbinder, E., Furth, N., Tanay, A., Barton, M., et al. p53 is essential for DNA methylation homeostasis in naïve embryonic stem cells, and its loss promotes clonal heterogeneity. Genes Dev 31 (2017), 959–972.
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20
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Deregulation of DNA methyltransferases and loss of parental methylation at the insulin-like growth factor II (Igf2)/H19 loci in p53 knockout mice prior to tumor development
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Park, I.Y., Sohn, B.H., Choo, J.H., Joe, C.O., Seong, J.K., Lee, Y.I., Chung, J.H., Deregulation of DNA methyltransferases and loss of parental methylation at the insulin-like growth factor II (Igf2)/H19 loci in p53 knockout mice prior to tumor development. J Cell Biochem 94 (2005), 585–596.
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Kruiswijk, F., Labuschagne, C.F., Vousden, K.H., p53 in survival, death and metabolic health: a lifeguard with a licence to kill. Nat Rev Mol Cell Biol 16 (2015), 393–405.
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Global genomic profiling reveals an extensive p53-regulated autophagy program contributing to key p53 responses
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Kenzelmann Broz, D., Mello, S.S., Bieging, K.T., Jiang, D., Dusek, R.L., Brady, C.A., Sidow, A., Attardi, L.D., Global genomic profiling reveals an extensive p53-regulated autophagy program contributing to key p53 responses. Genes Dev 27 (2013), 1016–1031.
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Emerging non-canonical functions and regulation by p53: p53 and stemness
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Olivos, D.J., Mayo, L.D., Emerging non-canonical functions and regulation by p53: p53 and stemness. Int J Mol Sci, 2016, 17.
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Olivos, D.J.1
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p53 regulates progenitor cell quiescence and differentiation in the airway
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McConnell, A.M., Yao, C., Yeckes, A.R., Wang, Y., Selvaggio, A.S., Tang, J., Kirsch, D.G., Stripp, B.R., p53 regulates progenitor cell quiescence and differentiation in the airway. Cell Rep 17 (2016), 2173–2182.
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McConnell, A.M.1
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Inactivation of p53 in breast cancers correlates with stem cell transcriptional signatures
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Mizuno, H., Spike, B.T., Wahl, G.M., Levine, A.J., Inactivation of p53 in breast cancers correlates with stem cell transcriptional signatures. Proc Natl Acad Sci U S A 107 (2010), 22745–22750.
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Krizhanovsky, V., Lowe, S.W., Stem cells: the promises and perils of p53. Nature 460 (2009), 1085–1086.
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Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations
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advance online publication
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Merkle, F.T., Ghosh, S., Kamitaki, N., Mitchell, J., Avior, Y., Mello, C., Kashin, S., Mekhoubad, S., Ilic, D., Charlton, M., et al. Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations. Nature, 2017 advance online publication.
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Nature
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Merkle, F.T.1
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Mello, C.6
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29
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69349100179
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Suppression of induced pluripotent stem cell generation by the p53–p21 pathway
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Hong, H., Takahashi, K., Ichisaka, T., Aoi, T., Kanagawa, O., Nakagawa, M., Okita, K., Yamanaka, S., Suppression of induced pluripotent stem cell generation by the p53–p21 pathway. Nature 460 (2009), 1132–1135.
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Hong, H.1
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30
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miR-34 miRNAs provide a barrier for somatic cell reprogramming
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Choi, Y.J., Lin, C.-P., Ho, J.J., He, X., Okada, N., Bu, P., Zhong, Y., Kim, S.Y., Bennett, M.J., Chen, C., et al. miR-34 miRNAs provide a barrier for somatic cell reprogramming. Nat Cell Biol 13 (2011), 1353–1360.
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Choi, Y.J.1
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Nakagawa, S., Hirose, T., Paraspeckle nuclear bodies — useful uselessness?. Cell Mol Life Sci 69 (2012), 3027–3036.
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Nakagawa, S.1
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Neat1 is a p53-inducible lincRNA essential for transformation suppression
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In this paper the authors identify Neat1 as a p53-induced lincRNA and demonstrate that Neat1 deficiency enhances transformation. Neat1 function is associated with its ability to preserve differentiation in oncogene-expressing cells.
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Mello, S.S., Sinow, C., Raj, N., Mazur, P.K., Bieging-Rolett, K., Broz, D.K., Imam, J.F.C., Vogel, H., Wood, L.D., Sage, J., et al. Neat1 is a p53-inducible lincRNA essential for transformation suppression. Genes Dev 31 (2017), 1095–1108 In this paper the authors identify Neat1 as a p53-induced lincRNA and demonstrate that Neat1 deficiency enhances transformation. Neat1 function is associated with its ability to preserve differentiation in oncogene-expressing cells.
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Mello, S.S.1
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Ferroptosis as a p53-mediated activity during tumour suppression
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This article shows that p53 can induce ferroptosis, an alternative cell death mechanism that could contribute to tumor suppression.
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Jiang, L., Kon, N., Li, T., Wang, S.-J., Su, T., Hibshoosh, H., Baer, R., Gu, W., Ferroptosis as a p53-mediated activity during tumour suppression. Nature 520 (2015), 57–62 This article shows that p53 can induce ferroptosis, an alternative cell death mechanism that could contribute to tumor suppression.
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Nature
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Jiang, L.1
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Acetylation is crucial for p53-mediated ferroptosis and tumor suppression
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Wang, S.J., Li, D., Ou, Y., Jiang, L., Chen, Y., Zhao, Y., Gu, W., Acetylation is crucial for p53-mediated ferroptosis and tumor suppression. Cell Rep 17 (2016), 366–373.
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Wang, S.J.1
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35
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An African-specific polymorphism in the TP53 gene impairs p53 tumor suppressor function in a mouse model
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Jennis, M., Kung, C.P., Basu, S., Budina-Kolomets, A., Leu, J.I., Khaku, S., Scott, J.P., Cai, K.Q., Campbell, M.R., Porter, D.K., et al. An African-specific polymorphism in the TP53 gene impairs p53 tumor suppressor function in a mouse model. Genes Dev 30 (2016), 918–930.
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Jennis, M.1
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36
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The tumor suppressor p53 limits ferroptosis by blocking DPP4 activity
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Xie, Y., Zhu, S., Song, X., Sun, X., Fan, Y., Liu, J., Zhong, M., Yuan, H., Zhang, L., Billiar, T.R., et al. The tumor suppressor p53 limits ferroptosis by blocking DPP4 activity. Cell Rep 20 (2017), 1692–1704.
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p53 and its mutants in tumor cell migration and invasion
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Muller, P.A.J., Vousden, K.H., Norman, J.C., p53 and its mutants in tumor cell migration and invasion. J Cell Biol 192 (2011), 209–218.
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p53 regulates epithelial–mesenchymal transition (EMT) and stem cell properties through modulating miRNAs
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Chang, C.-J., Chao, C.-H., Xia, W., Yang, J.-Y., Xiong, Y., Li, C.-W., Yu, W.-H., Rehman, S.K., Hsu, J.L., Lee, H.-H., et al. p53 regulates epithelial–mesenchymal transition (EMT) and stem cell properties through modulating miRNAs. Nat Cell Biol 13 (2011), 317–323.
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39
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