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Gene Review

Trp53  -  transformation related protein 53

Mus musculus

Synonyms: Cellular tumor antigen p53, P53, Tp53, Tumor suppressor p53, bbl, ...
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Disease relevance of Trp53

  • Mice inheriting two copies of this mutation (Trp53(515C/515C)) escape the early onset of thymic lymphomas that characterize Trp53-null mice [1].
  • Different Trp53 shRNAs produced distinct phenotypes in vivo, ranging from benign lymphoid hyperplasias to highly disseminated lymphomas that paralleled Trp53-/- lymphomagenesis in the E(mu)-Myc mouse [2].
  • In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma [3].
  • The tumor spectrum in Fancd2(-/-)/Trp53(+/-) mice included sarcomas expected in Trp53 heterozygotes, as well as mammary and lung adenocarcinomas that occur rarely in Trp53 heterozygotes [4].
  • Concomitant Trp53+/- mutation cooperated with Mist1(KrasG12D/+) to accelerate lethality and was associated with advanced histopathologic findings, including parenchymal liver metastasis [5].
  • Overexpression of sPRDM16 induces abnormal growth of stem cells and progenitors and cooperates with disruption of the p53 pathway in the induction of myeloid leukemia [6].
  • Activation of the p53(R172H) allele resulted in increased skin tumor formation, accelerated tumor progression, and induction of metastasis compared with deletion of p53 [7].
  • Ablation of Pin1, in addition to p53, accelerated the thymic hyperplasia, but the thymocytes in these Pin1-/-p53-/- mice did not infiltrate other organs [8].
  • E6, in the absence of E6AP retains an ability to induce epithelial hyperplasia, abrogate DNA damage responses and inhibit the induction of p53 protein following exposure to ionizing radiation [9].

Psychiatry related information on Trp53


High impact information on Trp53

  • Furthermore, we show that PRAK activates p53 by direct phosphorylation [15].
  • Therefore, NEDD4-1 is a potential proto-oncogene that negatively regulates PTEN via ubiquitination, a paradigm analogous to that of Mdm2 and p53 [16].
  • Yet Kras-transformed mouse colonocytes lacking p53 formed indolent, poorly vascularized tumors, whereas additional transduction with a Myc-encoding retrovirus promoted vigorous vascularization and growth [17].
  • Using the well-characterized Emu-myc lymphoma model, we show that p53 is spontaneously activated when restored in established Emu-myc lymphomas in vivo, triggering rapid apoptosis and conferring a significant increase in survival [18].
  • The cell death was preceded by aberrant accumulation of cell cycle regulators and increased genomic instability and could be partially rescued by removal of the tumor suppressor protein p53 [19].

Chemical compound and disease context of Trp53


Biological context of Trp53

  • Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice [1].
  • Deletion of the Trp53 tumor suppressor gene greatly accelerates Myc-induced lymphomagenesis, resulting in highly disseminated disease [2].
  • To define this role in vivo, we generated a Trp53 knock-in construct encoding a protein carrying mutations of two residues that are crucial for transactivation (L25Q,W26S) [25].
  • Our interest in the Gas-3 gene was prompted by our previously reported localization of the gene on the mouse chromosome 11.44 +/- 1.9 cM proximal to the Trp53 locus and by the finding, by others, that it codes for a myelin protein and that a point mutation in its fourth putative transmembrane region is associated with the trembler mutation [26].
  • Loss of heterozygosity occurs via mitotic recombination in Trp53+/- mice and associates with mammary tumor susceptibility of the BALB/c strain [27].

Anatomical context of Trp53

  • Mutational inactivation of Trp53 partially rescues the demethylated fibroblasts for up to five population doublings in culture [28].
  • Unexpectedly, elimination of one Trp53 allele completely rescues this embryonic lethality and restores normal mammary gland development [29].
  • To determine whether RNAi suppression of Trp53 could produce a similar phenotype, we introduced several Trp53 short hairpin RNAs (shRNAs) into hematopoietic stem cells derived from E(mu)-Myc transgenic mice, and monitored tumor onset and overall pathology in lethally irradiated recipients [2].
  • Crossing of Snm1 mutant mice with a Trp53 null mutant resulted in an increase in mortality and a restriction of the tumor type to lymphomas, particularly those of the thymus [30].
  • In multiple cell types, including mammary epithelial cells, abrogation of p53 (encoded by Trp53) function is associated with increased tumorigenesis [31].

Associations of Trp53 with chemical compounds

  • Double-mutant mice, which have greatly reduced Kit receptor tyrosine kinase activity and also lack Trp53, were generated and the affected cell lineages examined [32].
  • Treatment of 2-3-month-old Trp53(-/-), lacZ hybrid mice with the powerful mutagen ethyl nitrosourea (ENU) resulted in a higher number of mutations induced in the liver but not in the spleen, as compared to the Trp53(+/+), lacZ mice [33].
  • Although ectopic expression of wild-type p53 blocked cells in the G1 phase of the cell cycle, G1 arrest by isoleucine starvation, in a manner independent of p53, did not confer susceptibility to apoptosis [34].
  • MEFs lacking p53 or gadd45 genes exhibited decreased colony-forming ability after UV radiation and cisplatin compared to wild-type MEFs, indicating their sensitivity to DNA damage [35].
  • P53 was transiently phosphorylated at serine 23 during liver regeneration in an Atm-dependent manner [36].
  • Small interference RNA-mediated knockdown of p53 caused an inhibition of apoptosis following glucose depletion [37].

Physical interactions of Trp53

  • Rather, c-Jun regulates transcription of p53 negatively by direct binding to a variant AP-1 site in the p53 promoter [38].
  • We conclude that inactivation of ARF acts more broadly than that of p53 in connecting abrogation of the Rb pathway to tumorigenesis [39].
  • The Mdm2 oncoprotein forms a complex with the p53 tumor suppressor protein and inhibits p53-mediated regulation of heterologous gene expression [40].
  • BALB/c alleles for Prkdc and Cdkn2a interact to modify tumor susceptibility in Trp53+/- mice [41].
  • The promoter assays further confirmed the independency of p53-binding sites in the activation and linked UV-responsive transcriptional regulation of p21 to two Sp1 consensus binding sites within -61 bp of the transcription initiation site [42].
  • Newly discovered non-consensus p53-binding sites in p73, p53 and Egr1 promoters reveal inter-regulating networks and sustained expression by feedback loops in response to stress, resulting in prolonged expression of the p53 family of genes and efficient apoptosis [43].
  • The activated p38MAPK pathway stabilizes p53 via E2F1-mediated ARF expression, and also activates the transcriptional function of p53 by activating ATR [44].

Enzymatic interactions of Trp53

  • Polyomavirus large T antigen coprecipitates with p53 phosphorylated on serine 18 and also with p21Cip1/WAF1 [45].
  • DNAPK is normally activated by DNA dsbs and phosphorylates the p53 protein [46].
  • The co-precipitated complex by the anti-phospho-JNK antibody was capable of phosphorylating intrinsic or extrinsic p53 on Ser-15 [47].
  • We found that centrosomal p53 is poly(ADP-ribosyl)ated in vivo and centrosomal PARP-1 directly catalyzes poly(ADP-ribosyl)ation of p53 in vitro [48].
  • Recombinant wild-type mouse p53 was phosphorylated in vitro by activated recombinant p42-MAP kinase but not by inactive MAP kinase or by the activating protein, MAP kinase kinase [49].

Regulatory relationships of Trp53

  • The protracted latent period before the onset of frank disease likely reflects the ability of c-Myc to induce a p53-dependent apoptotic program that initially protects animals against tumor formation but is disabled when overtly malignant cells emerge [50].
  • The p19(ARF) tumor suppressor antagonizes Mdm2 to induce p53-dependent cell cycle arrest [51].
  • p53 is required for both radiation-induced differentiation and rescue of V(D)J rearrangement in scid mouse thymocytes [52].
  • This indicated that c-Jun controls hepatocyte proliferation by a p53/p21-dependent mechanism [53].
  • Here we show that the E2f3 mutation completely suppresses both the inappropriate proliferation and the p53-dependent apoptosis arising in the Rb mutant embryos [54].
  • These results indicate that p53 does not require p37(Ing1) to negatively regulate cell growth and offers genetic proof that Ing1 suppresses cell growth and tumorigenesis [55].
  • These data indicate that p73 is essential for suppressing polyploidy and aneuploidy when p53 is inactivated [56].
  • These results indicate that, at least in fibroblasts and thymocytes, p53-induced apoptosis proceeds principally via Noxa and Puma, with Puma having the predominant role in diverse cell types [57].
  • NPM enhances the expression of p53 target gene p21 and bax [58].

Other interactions of Trp53

  • Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles [59].
  • Mdm2 acts as a major regulator of the tumor suppressor p53 by targeting its destruction [60].
  • Thus, we have proposed that the reduction in mdm2 expression in Brca1 (5-6) mutants might lead to increased p53 activity [61].
  • Whereas induction of p53 involves events in the cell nucleus, the activation of transcription factors AP-1 and NF-kappaB by ultraviolet radiation is mediated through membrane-associated signalling proteins, ruling out a nuclear signal [62].
  • Induction of medulloblastomas in p53-null mutant mice by somatic inactivation of Rb in the external granular layer cells of the cerebellum [63].
  • NGF deprivation relieves XIAP by selectively degrading it, whereas DNA damage overcomes XIAP via a p53-mediated induction of Apaf-1 [64].
  • We find that inhibition of IGF-1R reduces p53 and Mdm2 translation through a gene-specific mechanism mediated by the respective 5' untranslated region of p53 and mdm2 messenger RNA [65].
  • A combined loss of MDM2 and p53 did not alter HIF-1alpha target expression compared with loss of p53 alone [66].
  • Unlike Mdm2 or most other p53 E3 ligases, MSL2-mediated p53 ubiquitination does not affect the stability of p53 [67].

Analytical, diagnostic and therapeutic context of Trp53

  • By Southern blotting, 96% (24 of 25) of BALB/c-Trp53(+/-) mammary tumors displayed LOH for Trp53 [27].
  • METHODS: Frequencies of murine bone marrow cells (BMCs) with the Lin(-)Sca-1(+)c-kit(+)CD34- phenotype were analyzed by flow cytometry, and were increased in mice with germ-line deletion of the Trp53 (Trp53(-/-)) gene but not in 25 other deletions of genes involved in cell cycling, development, cancer, or hematopoiesis [68].
  • Recipients of Trp53(-/-) donors had two to three times more Lin(-)Sca-1(+)c-kit(+)CD34(-) BMCs than recipients of Trp53(+/+) donors at five months after transplantation [68].
  • However, the mRNA expression of Trp53 and Cdkn1a (p21) after irradiation was not different among the organ types, and immunohistochemistry revealed that all the organs expressed these two proteins after irradiation [69].
  • C57BL/6 Trp53 heterozygous (N5) mice (p53+/- mice) show an increased sensitivity to tumorigenesis following exposure to genotoxic compounds and are being used as an alternate animal model for carcinogenicity testing [70].


  1. Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice. Liu, G., Parant, J.M., Lang, G., Chau, P., Chavez-Reyes, A., El-Naggar, A.K., Multani, A., Chang, S., Lozano, G. Nat. Genet. (2004) [Pubmed]
  2. An epi-allelic series of p53 hypomorphs created by stable RNAi produces distinct tumor phenotypes in vivo. Hemann, M.T., Fridman, J.S., Zilfou, J.T., Hernando, E., Paddison, P.J., Cordon-Cardo, C., Hannon, G.J., Lowe, S.W. Nat. Genet. (2003) [Pubmed]
  3. Susceptibility to astrocytoma in mice mutant for Nf1 and Trp53 is linked to chromosome 11 and subject to epigenetic effects. Reilly, K.M., Tuskan, R.G., Christy, E., Loisel, D.A., Ledger, J., Bronson, R.T., Smith, C.D., Tsang, S., Munroe, D.J., Jacks, T. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  4. Heterozygosity for p53 (Trp53+/-) accelerates epithelial tumor formation in fanconi anemia complementation group D2 (Fancd2) knockout mice. Houghtaling, S., Granville, L., Akkari, Y., Torimaru, Y., Olson, S., Finegold, M., Grompe, M. Cancer Res. (2005) [Pubmed]
  5. Mist1-KrasG12D knock-in mice develop mixed differentiation metastatic exocrine pancreatic carcinoma and hepatocellular carcinoma. Tuveson, D.A., Zhu, L., Gopinathan, A., Willis, N.A., Kachatrian, L., Grochow, R., Pin, C.L., Mitin, N.Y., Taparowsky, E.J., Gimotty, P.A., Hruban, R.H., Jacks, T., Konieczny, S.F. Cancer Res. (2006) [Pubmed]
  6. Overexpression of sPRDM16 coupled with loss of p53 induces myeloid leukemias in mice. Shing, D.C., Trubia, M., Marchesi, F., Radaelli, E., Belloni, E., Tapinassi, C., Scanziani, E., Mecucci, C., Crescenzi, B., Lahortiga, I., Odero, M.D., Zardo, G., Gruszka, A., Minucci, S., Di Fiore, P.P., Pelicci, P.G. J. Clin. Invest. (2007) [Pubmed]
  7. An inducible mouse model for skin cancer reveals distinct roles for gain- and loss-of-function p53 mutations. Caulin, C., Nguyen, T., Lang, G.A., Goepfert, T.M., Brinkley, B.R., Cai, W.W., Lozano, G., Roop, D.R. J. Clin. Invest. (2007) [Pubmed]
  8. Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1. Takahashi, K., Akiyama, H., Shimazaki, K., Uchida, C., Akiyama-Okunuki, H., Tomita, M., Fukumoto, M., Uchida, T. Oncogene (2007) [Pubmed]
  9. HPV16 E6 confers p53-dependent and p53-independent phenotypes in the epidermis of mice deficient for E6AP. Shai, A., Nguyen, M.L., Wagstaff, J., Jiang, Y.H., Lambert, P.F. Oncogene (2007) [Pubmed]
  10. Apoptogenic effects of black tea on Ehrlich's ascites carcinoma cell. Bhattacharyya, A., Choudhuri, T., Pal, S., Chattopadhyay, S., K Datta, G., Sa, G., Das, T. Carcinogenesis (2003) [Pubmed]
  11. Genetic interaction between expanded murine Hdh alleles and p53 reveal deleterious effects of p53 on Huntington's disease pathogenesis. Ryan, A.B., Zeitlin, S.O., Scrable, H. Neurobiol. Dis. (2006) [Pubmed]
  12. Apoptotic signaling proteins: possible participation in the regulation of vasopressin and catecholamines biosynthesis in the hypothalamus. Chernigovskaya, E.V., Taranukhin, A.G., Glazova, M.V., Yamova, L.A., Fedorov, L.M. Histochem. Cell Biol. (2005) [Pubmed]
  13. Inhibition of poly(ADP-ribose) polymerase activity accelerates T-cell lymphomagenesis in p53 deficient mice. Beneke, R., Möröy, T. Oncogene (2001) [Pubmed]
  14. Intracellular Abeta42 activates p53 promoter: a pathway to neurodegeneration in Alzheimer's disease. Ohyagi, Y., Asahara, H., Chui, D.H., Tsuruta, Y., Sakae, N., Miyoshi, K., Yamada, T., Kikuchi, H., Taniwaki, T., Murai, H., Ikezoe, K., Furuya, H., Kawarabayashi, T., Shoji, M., Checler, F., Iwaki, T., Makifuchi, T., Takeda, K., Kira, J., Tabira, T. FASEB J. (2005) [Pubmed]
  15. PRAK Is Essential for ras-Induced Senescence and Tumor Suppression. Sun, P., Yoshizuka, N., New, L., Moser, B.A., Li, Y., Liao, R., Xie, C., Chen, J., Deng, Q., Yamout, M., Dong, M.Q., Frangou, C.G., Yates, J.R., Wright, P.E., Han, J. Cell (2007) [Pubmed]
  16. NEDD4-1 Is a Proto-Oncogenic Ubiquitin Ligase for PTEN. Wang, X., Trotman, L.C., Koppie, T., Alimonti, A., Chen, Z., Gao, Z., Wang, J., Erdjument-Bromage, H., Tempst, P., Cordon-Cardo, C., Pandolfi, P.P., Jiang, X. Cell (2007) [Pubmed]
  17. Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster. Dews, M., Homayouni, A., Yu, D., Murphy, D., Sevignani, C., Wentzel, E., Furth, E.E., Lee, W.M., Enders, G.H., Mendell, J.T., Thomas-Tikhonenko, A. Nat. Genet. (2006) [Pubmed]
  18. Modeling the Therapeutic Efficacy of p53 Restoration in Tumors. Martins, C.P., Brown-Swigart, L., Evan, G.I. Cell (2006) [Pubmed]
  19. Deletion of DDB1 in Mouse Brain and Lens Leads to p53-Dependent Elimination of Proliferating Cells. Cang, Y., Zhang, J., Nicholas, S.A., Bastien, J., Li, B., Zhou, P., Goff, S.P. Cell (2006) [Pubmed]
  20. Chromosome 11 allelotypes reflect a mechanism of chemical carcinogenesis in heterozygous p53-deficient mice. Hulla, J.E., French, J.E., Dunnick, J.K. Carcinogenesis (2001) [Pubmed]
  21. Low levels of p53 are associated with resistance to tetrachlorodibenzo-p-dioxin toxicity in DBA/2 mice. Yang, A.L., Smith, A.G., Akhtar, R., Clothier, B., Robinson, S., MacFarlane, M., Festing, M.F. Pharmacogenetics (1999) [Pubmed]
  22. Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model. Fabris, V.T., Benavides, F., Conti, C., Merani, S., Lanari, C. Cancer Genet. Cytogenet. (2005) [Pubmed]
  23. Tumorigenesis in the multiple intestinal neoplasia mouse: redundancy of negative regulators and specificity of modifiers. Halberg, R.B., Katzung, D.S., Hoff, P.D., Moser, A.R., Cole, C.E., Lubet, R.A., Donehower, L.A., Jacoby, R.F., Dove, W.F. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  24. Distinct Effects of Annexin A7 and p53 on Arachidonate Lipoxygenation in Prostate Cancer Cells Involve 5-Lipoxygenase Transcription. Torosyan, Y., Dobi, A., Naga, S., Mezhevaya, K., Glasman, M., Norris, C., Jiang, G., Mueller, G., Pollard, H., Srivastava, M. Cancer Res. (2006) [Pubmed]
  25. The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality. Johnson, T.M., Hammond, E.M., Giaccia, A., Attardi, L.D. Nat. Genet. (2005) [Pubmed]
  26. Isolation and mapping to 17p12-13 of the human homologous of the murine growth arrest specific Gas-3 gene. Martinotti, A., Cariani, C.T., Melani, C., Sozzi, G., Spurr, N.K., Pierotti, M.A., Colombo, M.P. Hum. Mol. Genet. (1992) [Pubmed]
  27. Loss of heterozygosity occurs via mitotic recombination in Trp53+/- mice and associates with mammary tumor susceptibility of the BALB/c strain. Blackburn, A.C., McLary, S.C., Naeem, R., Luszcz, J., Stockton, D.W., Donehower, L.A., Mohammed, M., Mailhes, J.B., Soferr, T., Naber, S.P., Otis, C.N., Jerry, D.J. Cancer Res. (2004) [Pubmed]
  28. Loss of genomic methylation causes p53-dependent apoptosis and epigenetic deregulation. Jackson-Grusby, L., Beard, C., Possemato, R., Tudor, M., Fambrough, D., Csankovszki, G., Dausman, J., Lee, P., Wilson, C., Lander, E., Jaenisch, R. Nat. Genet. (2001) [Pubmed]
  29. Genetic interactions between tumor suppressors Brca1 and p53 in apoptosis, cell cycle and tumorigenesis. Xu, X., Qiao, W., Linke, S.P., Cao, L., Li, W.M., Furth, P.A., Harris, C.C., Deng, C.X. Nat. Genet. (2001) [Pubmed]
  30. Snm1-deficient mice exhibit accelerated tumorigenesis and susceptibility to infection. Ahkter, S., Richie, C.T., Zhang, N., Behringer, R.R., Zhu, C., Legerski, R.J. Mol. Cell. Biol. (2005) [Pubmed]
  31. Epithelial cell cycling predicts p53 responsiveness to gamma-irradiation during post-natal mammary gland development. Minter, L.M., Dickinson, E.S., Naber, S.P., Jerry, D.J. Development (2002) [Pubmed]
  32. Deficiency of Trp53 rescues the male fertility defects of Kit(W-v) mice but has no effect on the survival of melanocytes and mast cells. Jordan, S.A., Speed, R.M., Bernex, F., Jackson, I.J. Dev. Biol. (1999) [Pubmed]
  33. Age-related mutation accumulation at a lacZ reporter locus in normal and tumor tissues of Trp53-deficient mice. Giese, H., Snyder, W.K., van Oostrom, C., van Steeg, H., Dollé, M.E., Vijg, J. Mutat. Res. (2002) [Pubmed]
  34. Myc-mediated apoptosis requires wild-type p53 in a manner independent of cell cycle arrest and the ability of p53 to induce p21waf1/cip1. Wagner, A.J., Kokontis, J.M., Hay, N. Genes Dev. (1994) [Pubmed]
  35. p53-mediated DNA repair responses to UV radiation: studies of mouse cells lacking p53, p21, and/or gadd45 genes. Smith, M.L., Ford, J.M., Hollander, M.C., Bortnick, R.A., Amundson, S.A., Seo, Y.R., Deng, C.X., Hanawalt, P.C., Fornace, A.J. Mol. Cell. Biol. (2000) [Pubmed]
  36. Impaired hepatocyte survival and liver regeneration in Atm-deficient mice. Lu, S., Shen, K.C., Wang, Y., Brooks, S.C., Wang, Y.A. Hum. Mol. Genet. (2005) [Pubmed]
  37. Activation of AMP-activated protein kinase induces p53-dependent apoptotic cell death in response to energetic stress. Okoshi, R., Ozaki, T., Yamamoto, H., Ando, K., Koida, N., Ono, S., Koda, T., Kamijo, T., Nakagawara, A., Kizaki, H. J. Biol. Chem. (2008) [Pubmed]
  38. Control of cell cycle progression by c-Jun is p53 dependent. Schreiber, M., Kolbus, A., Piu, F., Szabowski, A., Möhle-Steinlein, U., Tian, J., Karin, M., Angel, P., Wagner, E.F. Genes Dev. (1999) [Pubmed]
  39. ARF mutation accelerates pituitary tumor development in Rb+/- mice. Tsai, K.Y., MacPherson, D., Rubinson, D.A., Nikitin, A.Y., Bronson, R., Mercer, K.L., Crowley, D., Jacks, T. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  40. The tumorigenic potential and cell growth characteristics of p53-deficient cells are equivalent in the presence or absence of Mdm2. Jones, S.N., Sands, A.T., Hancock, A.R., Vogel, H., Donehower, L.A., Linke, S.P., Wahl, G.M., Bradley, A. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  41. BALB/c alleles for Prkdc and Cdkn2a interact to modify tumor susceptibility in Trp53+/- mice. Blackburn, A.C., Brown, J.S., Naber, S.P., Otis, C.N., Wood, J.T., Jerry, D.J. Cancer Res. (2003) [Pubmed]
  42. UV radiation is a transcriptional inducer of p21(Cip1/Waf1) cyclin-kinase inhibitor in a p53-independent manner. Haapajärvi, T., Kivinen, L., Heiskanen, A., des Bordes, C., Datto, M.B., Wang, X.F., Laiho, M. Exp. Cell Res. (1999) [Pubmed]
  43. A network of p73, p53 and Egr1 is required for efficient apoptosis in tumor cells. Yu, J., Baron, V., Mercola, D., Mustelin, T., Adamson, E.D. Cell Death Differ. (2007) [Pubmed]
  44. Hepatitis B virus X protein via the p38MAPK pathway induces E2F1 release and ATR kinase activation mediating p53 apoptosis. Wang, W.H., Hullinger, R.L., Andrisani, O.M. J. Biol. Chem. (2008) [Pubmed]
  45. Induction and bypass of p53 during productive infection by polyomavirus. Dey, D., Dahl, J., Cho, S., Benjamin, T.L. J. Virol. (2002) [Pubmed]
  46. p53 induction, cell cycle checkpoints, and apoptosis in DNAPK-deficient scid mice. Gurley, K.E., Kemp, C.J. Carcinogenesis (1996) [Pubmed]
  47. Low levels of glutathione peroxidase 1 activity in selenium-deficient mouse liver affect c-Jun N-terminal kinase activation and p53 phosphorylation on Ser-15 in pro-oxidant-induced aponecrosis. Cheng, W.H., Zheng, X., Quimby, F.R., Roneker, C.A., Lei, X.G. Biochem. J. (2003) [Pubmed]
  48. Involvement of poly(ADP-Ribose) polymerase 1 and poly(ADP-Ribosyl)ation in regulation of centrosome function. Kanai, M., Tong, W.M., Sugihara, E., Wang, Z.Q., Fukasawa, K., Miwa, M. Mol. Cell. Biol. (2003) [Pubmed]
  49. Phosphorylation of the tumor suppressor protein p53 by mitogen-activated protein kinases. Milne, D.M., Campbell, D.G., Caudwell, F.B., Meek, D.W. J. Biol. Chem. (1994) [Pubmed]
  50. Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis. Eischen, C.M., Weber, J.D., Roussel, M.F., Sherr, C.J., Cleveland, J.L. Genes Dev. (1999) [Pubmed]
  51. p53-independent functions of the p19(ARF) tumor suppressor. Weber, J.D., Jeffers, J.R., Rehg, J.E., Randle, D.H., Lozano, G., Roussel, M.F., Sherr, C.J., Zambetti, G.P. Genes Dev. (2000) [Pubmed]
  52. p53 is required for both radiation-induced differentiation and rescue of V(D)J rearrangement in scid mouse thymocytes. Bogue, M.A., Zhu, C., Aguilar-Cordova, E., Donehower, L.A., Roth, D.B. Genes Dev. (1996) [Pubmed]
  53. c-Jun/AP-1 controls liver regeneration by repressing p53/p21 and p38 MAPK activity. Stepniak, E., Ricci, R., Eferl, R., Sumara, G., Sumara, I., Rath, M., Hui, L., Wagner, E.F. Genes Dev. (2006) [Pubmed]
  54. E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos. Ziebold, U., Reza, T., Caron, A., Lees, J.A. Genes Dev. (2001) [Pubmed]
  55. Deletion of p37Ing1 in mice reveals a p53-independent role for Ing1 in the suppression of cell proliferation, apoptosis, and tumorigenesis. Coles, A.H., Liang, H., Zhu, Z., Marfella, C.G., Kang, J., Imbalzano, A.N., Jones, S.N. Cancer Res. (2007) [Pubmed]
  56. p73 suppresses polyploidy and aneuploidy in the absence of functional p53. Talos, F., Nemajerova, A., Flores, E.R., Petrenko, O., Moll, U.M. Mol. Cell (2007) [Pubmed]
  57. In several cell types tumour suppressor p53 induces apoptosis largely via Puma but Noxa can contribute. Michalak, E.M., Villunger, A., Adams, J.M., Strasser, A. Cell Death Differ. (2008) [Pubmed]
  58. Nucleophosmin blocks mitochondrial localization of p53 and apoptosis. Dhar, S.K., St Clair, D.K. J. Biol. Chem. (2009) [Pubmed]
  59. Partial rescue of the prophase I defects of Atm-deficient mice by p53 and p21 null alleles. Barlow, C., Liyanage, M., Moens, P.B., Deng, C.X., Ried, T., Wynshaw-Boris, A. Nat. Genet. (1997) [Pubmed]
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