Relevant bibliographies by topics / P53

Academic literature on the topic 'P53'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "P53"

1

Li, Muyang, Fredrick Philantrope, Alexandra Diot, Jean-Christophe Bourdon, and Patricia Thompson. "A Novel Role of SMG1 in Cholesterol Homeostasis That Depends Partially on p53 Alternative Splicing." Cancers 14, no. 13 (July 2, 2022): 3255. http://dx.doi.org/10.3390/cancers14133255.

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SMG1, a phosphatidylinositol 3-kinase-related kinase (PIKK), essential in nonsense-mediated RNA decay (NMD), also regulates p53, including the alternative splicing of p53 isoforms reported to retain p53 functions. We confirm that SMG1 inhibition in MCF7 tumor cells induces p53β and show p53γ increase. Inhibiting SMG1, but not UPF1 (a core factor in NMD), upregulated several cholesterol pathway genes. SMG1 knockdown significantly increased ABCA1, a cholesterol efflux pump shown to be positively regulated by full-length p53 (p53α). An investigation of RASSF1C, an NMD target, increased following SMG1 inhibition and reported to inhibit miR-33a-5p, a canonical ABCA1-inhibiting miRNA, did not explain the ABCA1 results. ABCA1 upregulation following SMG1 knockdown was inhibited by p53β siRNA with greatest inhibition when p53α and p53β were jointly suppressed, while p53γ siRNA had no effect. In contrast, increased expression of MVD, a cholesterol synthesis gene upregulated in p53 deficient backgrounds, was sensitive to combined targeting of p53α and p53γ. Phenotypically, we observed increased intracellular cholesterol and enhanced sensitivity of MCF7 to growth inhibitory effects of cholesterol-lowering Fatostatin following SMG1 inhibition. Our results suggest deregulation of cholesterol pathway genes following SMG1 knockdown may involve alternative p53 programming, possibly resulting from differential effects of p53 isoforms on cholesterol gene expression.
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2

Gudikote, Jayanthi, Tina Cascone, Alissa Poteete, Piyada Sitthideatphaiboon, Sonia Patel, Yan Yang, Fahao Zhang, et al. "Abstract 5733: Targeting nonsense-mediated decay restores p53 function in HPV-associated head and neck cancers." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5733. http://dx.doi.org/10.1158/1538-7445.am2022-5733.

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Abstract HPV-positive (HPV+) head and neck squamous cell carcinoma (HNSCC) tumors typically have p53 loss due to the activity of the human papillomavirus (HPV)-encoded E6 protein and the E6-associated protein (HPVE6-AP) which mediate the degradation of wild-type (WT) p53 (p53α). The loss of p53 is thought to be a major contributor to the pathogenesis of HPV+ HNSCC, which comprise approximately 35% of all HNSCC. Currently, standard care for HPV+HNSCC includes radiation and chemotherapy. However long-term toxicity related to these treatments is a concern, and there is a need for newer therapeutic strategies. Previously, we reported that two alternatively spliced, functional truncated isoforms of p53 (p53β and p53γ, comprising of exons 1 to 9β or 9γ, respectively) are degraded by nonsense-mediated decay (NMD), a regulator of aberrant mRNA stability. Here, using HPV+HNSCC cell line models, we show that NMD inhibition rescues p53β/γ isoforms and activates p53 pathway. Furthermore, we show that p53β/γ isoforms are more stable compared to p53α in these cells, with reduced vulnerabililty to HPVE6-AP- mediated degradation, and that p53β/γ isoforms contribute to increased expression of p53 transcriptional targets p21 and PUMA following NMD inhibition. Consistent with p53 pathway activation, NMD inhibition enhanced radiosensitivity of HNSCC cells. NMD inhibition attenuated colony forming ability and disrupted cell cycle progression. To evaluate the therapeutic implications of NMD inhibition, we assessed the in vivo growth of HPV+ UMSCC47 tumors. Nude mice were injected with UMSCC47 cells either subcutaneously or orthotopically in the tongue and randomized to receive vehicle or with an NMD inhibitor. In both tumor models, we observed a significant reduction in tumor volume with NMD inhibition as compared to the vehicle-treated animals. To investigate whether NMD inhibition induced the expression of p53β/γ isoforms and activated the p53 pathway in vivo, we collected tumor tissues from animals and evaluated expression of p53 isoforms and transcriptional targets by RT-PCR. We observed increased expression of p53γ, p21, GADD45A and PUMA mRNAs in NMD inhibitor treated UMSCC47 tumors, compared to their respective vehicle treated controls. These results identify NMD inhibition as a novel therapeutic strategy for restoration of p53 function in major subgroups of p53-deficient HPV+ HNSCC tumors. Citation Format: Jayanthi Gudikote, Tina Cascone, Alissa Poteete, Piyada Sitthideatphaiboon, Sonia Patel, Yan Yang, Fahao Zhang, Lerong Li, Li Shen, Monique Nilsson, Phillip Jones, Jing Wang, Jean-Christophe Bourdon, Faye M. Johnson, John V. Heymach. Targeting nonsense-mediated decay restores p53 function in HPV-associated head and neck cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5733.
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3

Prikhod’ko, Grigori G., Yan Wang, Ella Freulich, Carol Prives, and Lois K. Miller. "Baculovirus p33 Binds Human p53 and Enhances p53-Mediated Apoptosis." Journal of Virology 73, no. 2 (February 1, 1999): 1227–34. http://dx.doi.org/10.1128/jvi.73.2.1227-1234.1999.

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ABSTRACT In vertebrates, p53 participates in numerous biological processes including cell cycle regulation, apoptosis, differentiation, and oncogenic transformation. When insect SF-21 cells were infected with a recombinant of the baculovirus Autographa californicanuclear polyhedrosis virus (AcMNPV) overexpressing human p53, p53 formed a stable complex with the product of the AcMNPV orf92, a novel protein p33. The interaction between p53 and p33 was further confirmed by immunoprecipitation studies. When individually expressed in SF-21 cells, human p53 localized mainly in the nucleus whereas baculovirus p33 displayed diffuse cytoplasmic staining and punctuate nuclear staining. However, coexpression of p33 with p53 resulted in exclusive nuclear localization of p33. In both SF-21 and TN-368 cells, p53 expression induced typical features of apoptosis including nuclear condensation and fragmentation, oligonucleosomal ladder formation, cell surface blebbing, and apoptotic body formation. Coexpression of p53 with a baculovirus inhibitor of apoptosis, p35, OpIAP, or CpIAP, blocked apoptosis, whereas coexpression with p33 enhanced p53-mediated apoptosis approximately twofold. Expression of p53 in SF-21 cells stably expressing OpIAP inhibited cell growth in the presence or absence of p33. Thus, human p53 can influence both insect cell growth and death and baculovirus p33 can modulate the death-inducing effects of p53.
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Haaland, Ingvild, Sigrun M. Hjelle, Håkon Reikvam, André Sulen, Anita Ryningen, Emmet McCormack, Øystein Bruserud, and Bjørn Tore Gjertsen. "p53 Protein Isoform Profiles in AML: Correlation with Distinct Differentiation Stages and Response to Epigenetic Differentiation Therapy." Cells 10, no. 4 (April 7, 2021): 833. http://dx.doi.org/10.3390/cells10040833.

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p53 protein isoform expression has been found to correlate with prognosis and chemotherapy response in acute myeloid leukemia (AML). We aimed to investigate how p53 protein isoforms are modulated during epigenetic differentiation therapy in AML, and if p53 isoform expression could be a potential biomarker for predicting a response to this treatment. p53 full-length (FL), p53β and p53γ protein isoforms were analyzed by 1D and 2D gel immunoblots in AML cell lines, primary AML cells from untreated patients and AML cells from patients before and after treatment with valproic acid (VPA), all-trans retinoic acid (ATRA) and theophylline. Furthermore, global gene expression profiling analysis was performed on samples from the clinical protocol. Correlation analyses were performed between p53 protein isoform expression and in vitro VPA sensitivity and FAB (French–American–British) class in primary AML cells. The results show downregulation of p53β/γ and upregulation of p53FL in AML cell lines treated with VPA, and in some of the patients treated with differentiation therapy. p53FL positively correlated with in vitro VPA sensitivity and the FAB class of AML, while p53β/γ isoforms negatively correlated with the same. Our results indicate that p53 protein isoforms are modulated by and may predict sensitivity to differentiation therapy in AML.
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Ashcroft, Margaret, Michael H. G. Kubbutat, and Karen H. Vousden. "Regulation of p53 Function and Stability by Phosphorylation." Molecular and Cellular Biology 19, no. 3 (March 1, 1999): 1751–58. http://dx.doi.org/10.1128/mcb.19.3.1751.

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ABSTRACT The p53 tumor suppressor protein can be phosphorylated at several sites within the N- and C-terminal domains, and several protein kinases have been shown to phosphorylate p53 in vitro. In this study, we examined the activity of p53 proteins with combined mutations at all of the reported N-terminal phosphorylation sites (p53N-term), all of the C-terminal phosphorylation sites (p53C-term), or all of the phosphorylation sites together (p53N/C-term). Each of these mutant proteins retained transcriptional transactivation functions, indicating that phosphorylation is not essential for this activity of p53, although a subtle contribution of the C-terminal phosphorylation sites to the activation of expression of the endogenous p21Waf1/Cip1-encoding gene was detected. Mutation of the phosphorylation sites to alanine did not affect the sensitivity of p53 to binding to or degradation by Mdm2, although alteration of residues 15 and 37 to aspartic acid, which could mimic phosphorylation, resulted in a slight resistance to Mdm2-mediated degradation, consistent with recent reports that phosphorylation at these sites inhibits the p53-Mdm2 interaction. However, expression of the phosphorylation site mutant proteins in both wild-type p53-expressing and p53-null lines showed that all of the mutant proteins retained the ability to be stabilized following DNA damage. This indicates that phosphorylation is not essential for DNA damage-induced stabilization of p53, although phosphorylation could clearly contribute to p53 stabilization under some conditions.
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Wienzek, Sandra, Judith Roth, and Matthias Dobbelstein. "E1B 55-Kilodalton Oncoproteins of Adenovirus Types 5 and 12 Inactivate and Relocalize p53, but Not p51 or p73, and Cooperate with E4orf6 Proteins To Destabilize p53." Journal of Virology 74, no. 1 (January 1, 2000): 193–202. http://dx.doi.org/10.1128/jvi.74.1.193-202.2000.

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ABSTRACT The p53 tumor suppressor protein represents a target for viral and cellular oncoproteins, including adenovirus gene products. Recently, it was discovered that several proteins with structural and functional homologies to p53 exist in human cells. Two of them were termed p51 and p73. We have shown previously that the E1B 55-kDa protein (E1B-55 kDa) of adenovirus type 5 (Ad5) binds and inactivates p53 but not p73. Further, p53 is rapidly degraded in the presence of E1B-55 kDa and the E4orf6 protein of this virus. Here, it is demonstrated that p51 does not detectably associate with E1B-55 kDa. While p53 is relocalized to the cytoplasm by E1B-55 kDa, p51's location is unaffected. Finally, p51 retains its full transcriptional activity in the presence of E1B-55 kDa. Apparently, p51 does not represent a target of Ad5 E1B-55 kDa, suggesting that the functions of p51 are distinct from p53-like tumor suppression. E1B-55 kDa from highly oncogenic adenovirus type 12 (Ad12) was previously shown to surpass the oncogenic activity of Ad5 E1B-55 kDa in various assay systems, raising the possibility that Ad12 E1B-55 kDa might target a broader range of p53-like proteins. However, we show here that Ad12 E1B-55 kDa also inhibits p53's transcriptional activity without measurably affecting p73 or p51. Moderate inhibition of p51's transcriptional activity was observed in the presence of the E4orf6 proteins from Ad5 and Ad12. p53 and Ad12-E1B-55 kDa colocalize in the nucleus and also in cytoplasmic clusters when transiently coexpressed. Finally, E1B-55 kDa and E4orf6 of Ad12 mediate rapid degradation of p53 with an efficiency comparable to that of the Ad5 proteins in human and rodent cells. Our results suggest that E1B-55 kDa of either virus type has similar effects on p53 but does not affect p73 and p51.
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Rocha, Sonia, Anthea M. Martin, David W. Meek, and Neil D. Perkins. "p53 Represses Cyclin D1 Transcription through Down Regulation of Bcl-3 and Inducing Increased Association of the p52 NF-κB Subunit with Histone Deacetylase 1." Molecular and Cellular Biology 23, no. 13 (July 1, 2003): 4713–27. http://dx.doi.org/10.1128/mcb.23.13.4713-4727.2003.

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ABSTRACT The p53 and NF-κB transcription factor families are important, multifunctional regulators of the cellular response to stress. Here we have investigated the regulatory mechanisms controlling p53-dependent cell cycle arrest and cross talk with NF-κB. Upon induction of p53 in H1299 or U-2 OS cells, we observed specific repression of cyclin D1 promoter activity, correlating with a decrease in cyclin D1 protein and mRNA levels. This repression was dependent on the proximal NF-κB binding site of the cyclin D1 promoter, which has been shown to bind the p52 NF-κB subunit. p53 inhibited the expression of Bcl-3 protein, a member of the IκB family that functions as a transcriptional coactivator for p52 NF-κB and also reduced p52/Bcl-3 complex levels. Concomitant with this, p53 induced a significant increase in the association of p52 and histone deacetylase 1 (HDAC1). Importantly, p53-mediated suppression of the cyclin D1 promoter was reversed by coexpression of Bcl-3 and inhibition of p52 or deacetylase activity. p53 therefore induces a transcriptional switch in which p52/Bcl-3 activator complexes are replaced by p52/HDAC1 repressor complexes, resulting in active repression of cyclin D1 transcription. These results reveal a unique mechanism by which p53 regulates NF-κB function and cell cycle progression.
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Terrier, Olivier, Virginie Marcel, Gaëlle Cartet, David P. Lane, Bruno Lina, Manuel Rosa-Calatrava, and Jean-Christophe Bourdon. "Influenza A Viruses Control Expression of Proviral Human p53 Isoforms p53β and Δ133p53α." Journal of Virology 86, no. 16 (May 30, 2012): 8452–60. http://dx.doi.org/10.1128/jvi.07143-11.

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Previous studies have described the role of p53 isoforms, including p53β and Δ133p53α, in the modulation of the activity of full-length p53, which regulates cell fate. In the context of influenza virus infection, an interplay between influenza viruses and p53 has been described, with p53 being involved in the antiviral response. However, the role of physiological p53 isoforms has never been explored in this context. Here, we demonstrate that p53 isoforms play a role in influenza A virus infection by using silencing and transient expression strategies in human lung epithelial cells. In addition, with the help of a panel of different influenza viruses from different subtypes, we also show that infection differentially regulates the expressions of p53β and Δ133p53α. Altogether, our results highlight the role of p53 isoforms in the viral cycle of influenza A viruses, with p53β and Δ133p53α acting as regulators of viral production in a p53-dependent manner.
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Ikawa, Shuntaro, Masuo Obinata, and Yoji Ikawa. "Human p53-p51 (p53-Related) Fusion Protein: A PotentBAXTransactivator." Japanese Journal of Cancer Research 90, no. 6 (June 1999): 596–99. http://dx.doi.org/10.1111/j.1349-7006.1999.tb00788.x.

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Fine, Robert L., Yuehua Mao, Richard Dinnen, Ramon V. Rosal, Anthony Raffo, Uri Hochfeld, Patrick Senatus, et al. "C-Terminal p53 Palindromic Tetrapeptide Restores Full Apoptotic Function to Mutant p53 Cancer Cells In Vitro and In Vivo." Biomedicines 11, no. 1 (January 5, 2023): 137. http://dx.doi.org/10.3390/biomedicines11010137.

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We previously demonstrated that a synthetic monomer peptide derived from the C-terminus of p53 (aa 361–382) induced preferential apoptosis in mutant p53 malignant cells, but not normal cells. The major problem with the peptide was its short half-life (half-life < 10 min.) due to a random coil topology found in 3D proton NMR spectroscopy studies. To induce secondary/tertiary structures to produce more stability, we developed a peptide modelled after the tetrameric structure of p53 essential for activation of target genes. Starting with the above monomer peptide (aa 361–382), we added the nuclear localization sequence of p53 (aa 353–360) and the end of the C-terminal sequence (aa 383–393), resulting in a monomer spanning aa 353–393. Four monomers were linked by glycine to maximize flexibility and in a palindromic order that mimics p53 tetramer formation with four orthogonal alpha helices, which is required for p53 transactivation of target genes. This is now known as the 4 repeat-palindromic-p53 peptide or (4R-Pal-p53p). We explored two methods for testing the activity of the palindromic tetrapeptide: (1) exogenous peptide with a truncated antennapedia carrier (Ant) and (2) a doxycycline (Dox) inducer for endogenous expression. The exogenous peptide, 4R-Pal-p53p-Ant, contained a His tag at the N-terminal and a truncated 17aa Ant at the C-terminal. Exposure of human breast cancer MB-468 cells and human skin squamous cell cancer cells (both with mutant p53, 273 Arg->His) with purified peptide at 7 µM and 15 µM produced 52% and 75%, cell death, respectively. Comparatively, the monomeric p53 C-terminal peptide-Ant (aa 361–382, termed p53p-Ant), at 15 µM and 30 µM induced 15% and 24% cell death, respectively. Compared to the p53p-Ant, the exogenous 4R-pal-p53p-Ant was over five-fold more potent for inducing apoptosis at an equimolar concentration (15 µM). Endogenous 4R-Pal-p53p expression (without Ant), induced by Dox, resulted in 43% cell death in an engineered MB468 breast cancer stable cell line, while endogenous p53 C-terminal monomeric peptide expression produced no cell death due to rapid peptide degradation. The mechanism of apoptosis from 4R-Pal-p53p involved the extrinsic and intrinsic pathways (FAS, caspase-8, Bax, PUMA) for apoptosis, as well as increasing reactive oxygen species (ROS). All three death pathways were induced from transcriptional/translational activation of pro-apoptotic genes. Additionally, mRNA of p53 target genes (Bax and Fas) increased 14-fold and 18-fold, respectively, implying that the 4R-Pal-p53p restored full apoptotic potential to mutant p53. Monomeric p53p only increased Fas expression without a transcriptional or translational increase in Fas, and other genes and human marrow stem cell studies revealed no toxicity to normal stem cells for granulocytes, erythrocytes, monocytes, and macrophages (CFU-GEMM). Additionally, the peptide specifically targeted pre-malignant and malignant cells with mutant p53 and was not toxic to normal cells with basal levels of WT p53.
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Dissertations / Theses on the topic "P53"

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Kommagani, Ramakrishna. "DIFFERENTIAL REGULATION OF VITAMIN D RECEPTOR (VDR) BY p53, p63 AND p73." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1239687284.

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Smolczyk, Yara [Verfasser], and Jörg [Akademischer Betreuer] Reichrath. "p53, Hautpigmentierung und Vitamin D : Untersuchungen zur Assoziation der Genvarianten (SNPs) von Mitgliedern der p53-Familie (p53, p63, p73) und der 25-Hydroxyvitamin- D-Serumkonzentration / Yara Smolczyk ; Betreuer: Jörg Reichrath." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2017. http://d-nb.info/1173163158/34.

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Billant, Olivier. "Utilisation de la levure S. cerevisiae pour déchiffrer les mécanismes de l'effet dominant-négatif affectant la famille de gènes suppresseurs de tumeurs p53, p63 et p73." Thesis, Brest, 2016. http://www.theses.fr/2016BRES0055/document.

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P53 est un gène suppresseur de tumeur ubiquitaire qui empêche la prolifération de cellules malignes chez l’humain. En réponse à des dommages à l’ADN ou à des stress cellulaires, p53 entraine l’arrêt du cycle cellulaire et initie la réparation des lésions du génome. Si ces réparations échouent, p53 déclenche alors la mort de la cellule endommagée par apoptose. De plus, p53 présente une forte homologie avec deux autres gènes suppresseurs de tumeur : p63 et p73. Ces trois protéines forment une famille de facteurs de transcription qui protège l’organisme contre le développement de tumeurs. Ce système de défense est enrichi par les multiples isoformes de p53, p63 et p73 dont les rôles sont encore mal décrits. La neutralisation de la fonction de suppression de tumeur de p53, p63 et p73 est un mécanisme clef du développement tumoral auquel participent les mutants hotspots de p53 ainsi que certaines isoformes de p53, p63 et p73 par un effet dominant-négatif. Toutefois, de nombreuses zones d’ombre limitent notre compréhension de ce phénomène. Tout d’abord, l’identification des membres de la famille de p53 impliqués dans l’effet dominant-négatif reste incomplète. Ensuite, les mécanismes responsables de l’effet dominant-négatif sont débattus, suite notamment à l’émergence d’une nouvelle hypothèse impliquant un mécanisme de type prion. Enfin, l’effet dominant-négatif de la famille de p53 pourrait également être mis en cause dans d’autres types de pathologies comme les syndromes développementaux associés à des mutations de p63. Au cours de cette thèse, j’ai étudié l’impact fonctionnel des mutations hotspots de p53 ainsi que celui des principales isoformes de la famille de p53 sur l’activité transcriptionnelle des isoformes actives de p53, p63 et p73. En utilisant comme modèle d’étude un eucaryote simple, la levure S. cerevisiae, nous avons pu démontrer que l’effet dominant-négatif des mutants et isoformes de la famille de p53 repose sur la formation d’hétéro-tétramères entre formes actives et inactives de ces protéines et n’implique pas de mécanisme de type prion. De plus nos travaux ont montré que certains mutants de p53 interfèrent avec les isoformes actives de p63 et p73 par un mécanisme partiellement basé sur la tétramérisation. En outre, nos résultats préliminaires suggèrent que les mutants de p63 impliqués dans les syndromes développementaux EEC, ADULT et NSCL1 exercent également un effet dominant-négatif similaire à celui des mutants de p53. L’identification des mécanismes de l’effet dominant-négatif observé au sein de la famille de p53 permet d’envisager de nouvelles cibles thérapeutiques tant dans les cancers que dans certaines maladies rares du développement humain
P53 is a ubiquitous tumor suppressor gene that prevents damaged cells from proliferating. Following DNA damage or cellular stress, p53 induces a cell cycle arrest and initiates an attempt to repair the lesions. If the repair fails, p53 triggers the apoptosis of the cell. p53 shares a high homology with two other tumor suppressor genes: p63 and p73. Together they form a family of transcription factors, which are actively protecting the organism from tumor development. This defense network is enriched by multiple N-terminal and C-terminal isoforms of p53, p63 and p73. The loss of p53, p63 and p73 tumor suppression function is a key step of cancer progression. Mutants of p53 and isoforms of p53, p63 and p73 often exhibit a dominant-negative behavior resulting in the loss of p53 tumor suppression activity. However, the extent of the dominant-negative effect within p53 family remains unclear. The mechanisms behind the dominant-negative effect are also debated due to the recent emergence of a prion-like hypothesis. Finally, the dominant-negative effect of p53 family members could be involved in other pathologies such as p63-related developmental syndromes During this PhD, I studied the functional consequences of hotspot mutations of p53 and of the main isoforms of the p53 family on the transcriptional activity of p53, p63 and p73. Using the naïve eukaryotic model S. cerevisiae we have demonstrated that the dominant-negative effect of mutants and isoforms of the p53 family relies on the formation of hetero-tetramers between functional and non-functional members of the family but not on a prion-like mechanism. In addition, certain p53 mutants are able to interfere with p63 and p73 isoforms though a mechanism that is only partially based on tetramerization. Of note, we obtained preliminary results suggesting that mutants of p63, which are involved in EEC, ADULT and NSCL1 developmental syndromes, behave like dominant-negative hotspot mutants of p53. The identification of the mechanisms of the dominant-negative effect occurring within p53 family could lead to new therapeutic targets both in cancer and in rare developmental syndromes.1 EEC : ectrodactyly, ectodermal dysplasia and cleft lip/palate syndrome, ADULT : acro-dermato-ungual-lacrimal-tooth syndrome, NSCL : non-syndromic cleft lip
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Huang, Vera. "Interactions of p53 and p73 with human promoters." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3283559.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed November 21, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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5

Gillardin, Pierre. "Régulation épigénétique et protéique de p73 dans le Myélome Multiple." Thesis, Nantes, 2017. http://www.theses.fr/2017NANT1037/document.

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Les anomalies de TP53, que sont la délétion génique associée ou non à des mutations somatiques, demeurent un facteur de résistance au traitement dans le Myélome Multiple (MM) malgré l’introduction de nouveaux agents thérapeutiques. Pour contourner les anomalies de TP53, nous avons étudié la possibilité d’activer p73, un membre de la famille de p53, qui n’est pas fréquemment muté dans les cancers. Nous avons étudié l’expression, la méthylation et la régulation de TP73 dans une collection de lignées de MM sauvages ou déficientes pour p53. Nous montrons que TP73 est rarement exprimé et surtout dans les lignées TP53 sauvage. Nous avons étudié la méthylation de l’ilot CpG situé en amont du gène par MS-PCR et montré que l’absence d’expression correspond à son hyperméthylation, qui peut néanmoins être réversée par la décitabine, un inhibiteur de la méthylation. Malgré l’augmentation d’expression de TP73, la décitabine ne permet pas une expression protéique significative de p73. Pour étudier la régulation de p73, nous avons utilisé des agents alkylants, des inhibiteurs de MDM2 et du protéasome. Nous montrons que les nutlin3a et MG132, ne stabilisent pas p73 mais diminuent son expression constitutive. Les agents alkylants induisent une augmentation de p73 mais uniquement dans les lignées TP53 sauvage et l’extinction de p53 par ARN interférence inhibe cette régulation. Dans les lignées déficientes pour p53, la décitabine augmente l’expression génique mais le melphalan ne permet pas de stabilisation de la protéine. L’ensemble de nos résultats montre que TP73 n’apparaît pas être un bon candidat pour contourner les anomalies de TP53
TP53 deficiency remains a major adverse event in Multiple Myeloma despite therapeutic progresses. p73, a member of p53 family, is very rarely mutated and has been poorly studied in myeloma. Using human myeloma cell lines with different TP53 status, we assessed methylation, expression and regulation of TP73. We report that TP73 is silenced by methylation and that decitabine increases its expression, which remains however insufficient for significant protein expression. Alkylating drugs increase expression of TP73 only in TP53wt cells and fail to synergize with decitabine in p53 deficient cells. On the other hand, MG132 and nutlin-3a don’t stabilize p73 in response to in TP53wt p73 positive cell lines. TP73 does not appear as a promising target for bypassing p53 deficiency in Multiple Myeloma
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Trnkus, Amanda. "Comparing wild-type p53 and a p53 isoform, p47." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107723.

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p53 is a tumor suppressor protein that is mutated in over 50% of human cancers. Although tightly regulated under normal conditions, this protein is quickly activated in response to a multitude of cellular stresses, inducing several downstream pathways such as cell cycle arrest, apoptosis, and senescence. p47 is an N-terminal truncated isoform made by alternative splicing of the p53 gene or from an alternative initiation site for translation, likely through cap-independent translation via an IRES. The objective of this study is to better understand the functions of p47 and to determine its structure and whether it can inhibit p53. p53 is part of a larger homologous family of proteins, including p63 and p73 – both of which contain their own N-terminally truncated isoforms. Having a complete understanding of all these proteins' roles is essential to better understand how cancer originates, progresses, and which pathways are affected. Whether p47 is a negative regulator of p53 or not is currently being disputed due to conflicting results. Evidence in this study suggests that, although p47 shares a structural conformation similar to mutant p53R175H, overall it does not negatively regulate p53. p47 is able to induce growth suppression of cancer cells and does not impair p53's suppression of growth or p53's induction of p21, nor does p47 alter the nuclear localization of p53. These results argue that p47 is not a negative regulator of p53.
La protéine p53 est un gène suppresseur de tumeurs qui est muté dans plus de 50% des cancers humains. Quoique cette protéine soit étroitement contrôlée, elle peut être rapidement activée en réponse à une variété de stress cellulaires et mène à l'activation de plusieurs voies métaboliques telles que l'arrêt du cycle cellulaire, l'apoptose et la sénescence. p47 est un isoforme de p53 tronqué à l'extrémité N-terminale. La protéine p47 est générée soit par épissage alternatif de p53, soit par initiation de la traduction à un site alternatif, probablement par un mécanisme indépendant de la coiffe en 5' via un site d'entrée interne ribosomal (séquence IRES).Le but de ce projet est de mieux comprendre les fonctions de p47, notamment en déterminant sa structure et si p47 peut inhiber p53. p53 appartient à une grande famille de protéines homologues qui inclut p63 et p73, deux protéines qui ont leurs propres isoformes tronqués à l'extrémité N-terminale. Connaître le rôle de ces protéines est essentiel pour mieux comprendre comment le cancer apparaît, progresse, et les voies métaboliques qui y sont affectées. A cause de résultats contradictoires dans la littérature scientifique, il n'est pas clair si p47 peut inhiber p53. Les résultats présentés dans cette étude suggèrent que, bien que p47 a une structure semblable au mutant p53R175H de p53, p47 ne contrôle pas p53. p47 peut bloquer la croissance de cellules cancéreuses et n'affecte pas le blocage de croissance causé par p53, l'induction de p21 par p53, ni la localisation nucléaire de p53. Ces résultats indiquent que p47 n'est pas un régulateur négatif de p53.
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Rutherford, Jodie. "Germline p53 mutations : characterisation and mechanisms of P53 dysfunction." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252278.

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Tweddle, Deborah Anne. "The role of p53 and p53 regulated proteins in neuroblastoma." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246680.

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Jaggi, Gaurav. "Rescuing p53 function : screening and characterization of p53 stabilizing drugs." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608405.

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Choi, Sang H. "Study of p53 Gain of Function Mutations in p53-null Astrocytes." VCU Scholars Compass, 2000. http://scholarscompass.vcu.edu/etd/4420.

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A number of recent studies suggest that expression of mutant p53 with mutations in certain codons show a gain of function and some of the characteristics of an oncoprotein. In order to study gain of function mutation and eliminate the potential of a dominant negative interaction with endogenous wild type p53 protein, p53 knockout mouse astrocytes were used. A retrovirus system was used to introduce mutant p53 genes into these p53-null astrocytes. Immunohistochemical staining and western blot experiments showed the expression of mutant p53 protein in these cells after infection with the mutant p53 retroviruses. Cell growth experiment did not suggest growth advantages for mutant p53 expressing astrocytes over vector control cells. Data from clonogenic survival assays following exposure to etoposide or cisplatin suggested that mutant p53 expressing cells with a point mutation at codon 273 may be resistant to apoptosis induced by etoposide. In contrast, p53 with a point mutation at codon 248 may sensitize cells to the apoptotic effects of etoposide and cisplatin.
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Books on the topic "P53"

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Ayed, Ayeda, and Theodore Hupp. p53. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-8231-5.

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Deb, Sumitra, and Swati Palit Deb. p53 Protocols. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592594085.

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Deb, Sumitra, and Swati Palit Deb, eds. p53 Protocols. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-236-0.

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name, No. p53 protocols. Totowa, NJ: Humana Press, Inc., 2003.

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Sumitra, Deb, and Deb Swati Palit, eds. p53 protocols. Totowa, N.J: Humana Press, 2003.

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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. p53 Suppressor Gene. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1.

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A, Maxwell Steven, and Roth Jack A, eds. p53 suppressor gene. New York: Springer-Verlag, 1995.

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Hainaut, Pierre, Magali Olivier, and Klas G. Wiman, eds. p53 in the Clinics. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3676-8.

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Hainaut, Pierre, and Klas G. Wiman, eds. 25 Years of p53 Research. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/978-1-4020-2922-6.

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Hainaut, Pierre, and Klas G. Wiman, eds. 25 Years of p53 Research. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/1-4020-2922-5.

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Book chapters on the topic "P53"

1

McKeon, Frank, and Annie Yang. "P53, P63, and P73: Internecine Relations?" In 25 Years of p53 Research, 209–22. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-2922-6_9.

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Duncan, Aundrietta D., Wen-Wei Tsai, and Michelle Craig Barton. "p53." In Signaling Pathways in Liver Diseases, 364–73. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118663387.ch26.

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Chiaravalli, Anna Maria, and Rebecca D’Amato Pascarella. "p53." In Encyclopedia of Pathology, 1–3. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5093-1.

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Menendez, Daniel, Thuy-Ai Nguyen, Michael A. Resnick, and Carl W. Anderson. "p53." In Encyclopedia of Signaling Molecules, 3740–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_57.

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Tsai, Wen-Wei, and Michelle Craig Barton. "p53." In Signaling Pathways in Liver Diseases, 345–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_23.

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Menendez, Daniel, Thuy-Ai Nguyen, Michael A. Resnick, and Carl W. Anderson. "p53." In Encyclopedia of Signaling Molecules, 1–16. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_57-1.

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Chiaravalli, Anna Maria, and Rebecca D’Amato Pascarella. "p53." In Endocrine Pathology, 591–93. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5093.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "p53." In Encyclopedia of Signaling Molecules, 1332–45. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_57.

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Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis, et al. "p53." In Encyclopedia of Exercise Medicine in Health and Disease, 690. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2913.

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Olivier, Magali, Audrey Petitjean, Claude de Caron Fromentel, and Pierre Hainaut. "TP53 Mutations in Human Cancers: Selection versus Mutagenesis." In p53, 1–18. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-8231-5_1.

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Conference papers on the topic "P53"

1

LANE, DAVID. "THE P53 PATHWAY." In Proceedings of the 18th International Conference. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2007. http://dx.doi.org/10.1142/9781860949852_0018.

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Tian, Xiaobing, Nagib Ahsan, and Wafik S. El-Deiry. "Abstract 1284: P53-independent restoration of p53 pathway in tumors with mutated p53 through ATF4 transcriptional modulation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1284.

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Shin, Yong-Jun, Steven M. Lipkin, Brandon Hencey, and Xiling Shen. "Disturbance Rejection Helps Modulate the p53 Oscillation." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6046.

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Designing a system that adequately processes the input and that rejects the effects of disturbance is a central theme in feedback control theory. In this paper, we use the concept of “disturbance rejection” to analyze the oscillatory behavior of p53, a well-known tumor suppressor protein. Our analysis reveals that the p53 oscillation is not completely dictated by the p53-MDM2 negative feedback loop—it is also modulated by periodic DNA repair-related fluctuations. According to our disturbance rejection model, the feedback loop normally filters the effects of noise and fluctuations on p53, but upon DNA damage, it stops performing the filtering function so that DNA repair-related fluctuations can modulate the p53 oscillation. Our analysis suggests that the overexpression of MDM2, observed in many types of cancer, can make the feedback mechanism less responsive to the modulating signals after DNA damage occurs.
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Воропаева, О. Ф., К. С. Гаврилова, and С. Д. Сенотрусова. "MATHEMATICAL MODELING OF THE DYNAMICS OF THE DEGENERATIVE DISEASES BIOMARKERS NETWORK." In XVII Российская конференция “Распределенные информационно-вычислительные ресурсы: Цифровые двойники и большие данные”. Crossref, 2019. http://dx.doi.org/10.25743/ict.2019.15.81.028.

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Выполнен сопоставительный анализ ряда известных математических моделей функционирования сигнального пути белка p53, основанных на разных биологических идеализациях процесса. Даны оценки области применимости моделей. Обнаружены бифуркации Андронова-Хопфа и Неймарка-Сакера в диапазонах фазовых состояний p53 и его ингибиторов, соответствующих нормальной реакции сигнального пути p53 на стресс. Исследованы варианты гипотетических терапевтических противораковых стратегий. A comparative analysis of a number of known mathematical models of the p53 protein signaling pathway functioning based on different biological idealizations of the process is performed. Estimates of the applicability of the models are given. Andronov-Hopf and NeimarkSaker bifurcations were found in the ranges of p53 phase states and its inhibitors corresponding to the normal response of the p53 signaling pathway to stress. Variants of hypothetical therapeutic anticancer strategies were investigated.
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Zhang, Xin, Kesheng Wang, Hailian Sheng, Tingting Li, Gang Chen, Fei Chen, Qinwan Wang, Zhihong Cheng, Zhiqin Wang, and Zeguang Han. "Abstract 1008: IRTKS suppresses p53 activity through promoting MDM2 mediated p53 monoubiquitination." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1008.

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Atha, Donald H., and Vytas Reipa. "Abstract 4899: Development of a quantitative measurement of p53 – p53 antibody interactions." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4899.

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Mori, Jinichi, Paulysally Lo, Chizu Tanikawa, Yusuke Nakamura, and Koichi Matsuda. "Abstract 1228: Identification of a novel p53 target regulating p53-induced apoptotic pathway." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1228.

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Yang, Hee Jung, Seong Jun Cho, Jin Zhang, Wensheng Yan, and Xinbin Chen. "Abstract 675: Ninjurin1, a target of p53, modulates p53-dependent tumor suppressionin vivo." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-675.

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Morton, Derrick Jerone, Divya Patel, Jugal Joshi, Pankaj Sharma, Ashley Knowell, Aisha Hunt, and Jaideep Chaudhary. "Abstract 1219: ID4 and p53 cross-talk promotes restoration of mutant-p53 transcriptional activity." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1219.

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Dai, Mushui, Krishna Chauhan, Yingxiao Chen, and Xiao-Xin Sun. "Abstract 3536: SENP1 is a p53 deSUMOylating enzyme and its depletion induces p53 activity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3536.

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Reports on the topic "P53"

1

Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437662.

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Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada456200.

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Yang, Annie. Role of the p53 Tumor Suppressor Homolog, p63, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada471497.

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McNaughton-Harms, Kelly L. Mechanisms of p53-Mediated Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada456010.

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McNaughton, Kelly L. Mechanisms of p53-Mediated Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada435101.

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Harms, Kelly L. Mechanisms of p53-Mediated Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada468053.

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Abela, Brian C., and Kuan Liu. Characterization of a p53 Regulatory Domain. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada405271.

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Abela, Brian C. Characterization of a p53 Regulatory Domain. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada367640.

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Abela, Brian C., and Xuan Liu. Characterization of a p53 Regulatory Domain. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada391313.

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Liu, Xuan, and Brian C. Abela. Characterization of a p53 Regulatory Domain. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392350.

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