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Dissertations / Theses on the topic 'P53 tumour suppressor protein'

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Published: 4 June 2021

Last updated: 25 January 2023

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1

Marston, Nicola Jane. "Mutational analysis of the tumour suppressor protein, p53." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387679.

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2

Protopopova, Marina. "Modulation of activity of the tumour suppressor p53 by small molecules and damaged DNA /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-926-9/.

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3

Husaini, Roslina. "Towards the Investigation of the Effects of Nitration on the Activity of the Human p53 Tumour Suppressor Protein. Nitration of the p53 Tumour Suppressor Protein." Thesis, University of Bradford, 2014. http://hdl.handle.net/10454/14788.

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Upon responding to cellular stress, p53 protein becomes stabilised and acts as a transcription factor mainly resulting from phosphorylation and acetylation of the protein. Nitration of p53 protein is poorly characterised by comparison with phosphorylation and acetylation. The main aim of this work was to study the effects of nitration on p53 functional activities and on p53-MDM2 protein-protein interactions. Preliminary work was to characterise the nitration of p53 protein over-expressed in E. coli BL21(DE3) which was then purified by a series of column chromatography. GST-MDM2 protein along w

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4

Cuella-Martin, Raquel. "Molecular regulation of p53-dependent tumour suppressor responses by the p53 binding protein 1." Thesis, University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:7b2e64f3-bda4-4c3c-aeaf-d27393b7bc07.

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The tumour suppressor p53 binding protein 1 (53BP1), a fundamental node in DNA double strand break (DSB) repair, was identified as a p53-interacting protein over two decades ago. However, its contribution to p53-dependent responses has remained largely enigmatic. Here, using a combination of detailed structure-function approaches and in vivo analyses I aim to unravel this aspect of 53BP1 functionality. I showed 53BP1 to enhance genome-wide p53-dependent transactivation events in response to multiple stress stimuli. Oligomerised 53BP1 relies on the tandem BRCT domain, dispensable for 53BP1-driv

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5

Rajagopalan, Sridharan. "Biophysical characterization of tumour suppressor p53 and its protein-interaction network." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608428.

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6

Jowsey, Paul Andrew. "The role of poly(ADP-ribose) polymerase-1 in the MDM2-p53 DNA damage response pathway." Thesis, University of Newcastle Upon Tyne, 2003. http://hdl.handle.net/10443/1005.

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p53 is a tumour suppressor protein that is stabilised and activated by DNA damage. DNA damage-induced p53 is able to bring about either cell cycle arrest or apoptosis by the induction of p53-responsive genes such as mdm2 and p21 waf-I. Mdm2 regulates p53 function by blocking the transcriptional transactivation domain of p53 and also by targeting p53 for degradation via an ubiquitin-mediated pathway. Increases in the levels and activity of p53 are brought about by post-translational modifications. The most widely studied modification of p53 is phosphorylation, mediated by several DNA damageacti

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7

Liu, Geng. "Control of the p53 tumour suppressor protein through the NEDD8 conjugation pathway." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505643.

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8

Mee, Trevor Richard. "Analysis of the proteolytic cleavage reaction of the tumour suppressor protein p53." Thesis, University of York, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310987.

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9

Baloglu, Cetin. "N terminal and DNA binding domain interactions of tumour suppressor protein p53." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608567.

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10

Heberling, Matthew Michael. "Improving stability of tumor suppressor protein, p53." Connect to resource, 2007. http://hdl.handle.net/1811/28445.

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Thesis (Honors)--Ohio State University, 2007.<br>Title from first page of PDF file. Document formatted into pages: contains 25 p.; also includes graphics. Includes bibliographical references (p. 23-25). Available online via Ohio State University's Knowledge Bank.

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11

Marcar, Lynnette Nongkynrih. "Inhibition of p53 tumour suppressor function by tumour associated MAGE-A proteins." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521696.

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12

Lilyestrom, Wayne. "The structure of the complex containing the oncoprotein SV40 large tumour antigen bound to the p53 tumor suppressor /." Connect to full text via ProQuest. IP filtered, 2006.

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Thesis (Ph.D. in Biochemistry) -- University of Colorado, 2006.<br>Typescript. Includes bibliographical references (leaves 69-83). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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13

Abdul, Hamid Nazefah. "Intracellular relocalisation of the p53 tumour suppressor protein by the HPV 16 E2." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528100.

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14

Marini, Wanda. "Comparing mutant p53 and a wild-type p53 isoform, p47 : rationale for the selection of mutant p53 in tumours." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116033.

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One of the major unresolved questions in cancer biology is why the majority of tumour cells express mutant p53 proteins. p53 is considered the prototype tumour suppressor protein, whose inactivation is the most frequent single genetic event in human cancer (Bourdon et al., 2005). Genetically-engineered p53-null knockout mice acquire multiple tumours very early on in life and human Li-Fraumeni families who carry germline mutations in p53 are highly cancer-prone (reviewed in Vousden and Lane, 2007). p53 mutant proteins have been found to acquire novel functions that promote cancer cell prolifera

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15

Hafsi, Hind. "N-terminal isoforms of the p53 tumour suppressor protein : effects on p53 transcriptional activity and expression in cutaneous melanoma." Phd thesis, Université Claude Bernard - Lyon I, 2012. http://tel.archives-ouvertes.fr/tel-00995000.

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The p53 tumour suppressor protein has a highly complex pattern of regulation at transcriptional and posttranslationallevels. The discovery of p53 isoforms has added another layer of complexity to the mechanisms thatregulate p53 functions. Indeed, p53 is expressed as 12 isoforms that differ in their N- and C-terminus due toalternative splicing, promoter or codon initiation usage. So far, there is limited understanding of the patterns ofexpression and of the functions of each of these isoforms.In this Thesis, we have focused on the two major p53 N-terminal isoforms, Δ40p53 and Δ133p53. We havean

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16

Serpi, R. (Raisa). "Mechanism of benzo(a)pyrene-induced accumulation of p53 tumour suppressor protein in mouse." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514270398.

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Abstract The tumour suppressor gene TP53 is the most commonly mutated gene in human cancers. The protein it codes, p53, becomes activated as a response to stress signals. When activated, p53 binds to DNA and affects the transcription of its target genes. They then cause cell cycle arrest, DNA repair and/or induction of programmed cell death, thus preventing mutations and cancer. Specific mutations in TP53 are associated with exposure to certain carcinogens, such as polycyclic aromatic hydrocarbons (PAHs). These environmental chemical carcinogens are formed through incomplete combustion of orga

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17

O'Connor, Daniel Jeremy. "The investigation of cellular proteins which influence p53 tumour suppressor function." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314214.

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18

Kernohan, Neil M. "Regulation of complex formation between the tumour suppressor protein p53 and SV40 large T antigen." Thesis, City University London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287647.

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19

Dowell, Stephanie Patricia. "Studies of the p53 tumour suppressor gene and related proteins in cytopathology." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336432.

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20

Jooste, Lauren Sarah. "In vitro investigation of the ubiquitination and degradation of p53 by Murine Double Minute 2 (MDM2) and Retinoblastoma Binding Protein 6 (RBBP6)." University of the Western Cape, 2015. http://hdl.handle.net/11394/5051.

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>Magister Scientiae - MSc<br>P53 is one of the most important tumour suppressor proteins in the body which protects the cell against the tumourigenic effects of DNA damage by initiating processes such as apoptosis, senescence and cell cycle arrest. Regulation of p53 is key — so that the abovementioned processes are not initiated inappropriately. The principle negative regulator of p53 is Murine Double Minute 2 (MDM2), a RING finger-containing protein which catalyses the attachment of lysine48-linked poly-ubiquitin chains, targeting it for degradation by the 26S proteasome. It has been found to

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21

Xie, Tian. "Scintillation proximity assay (SPA) measuring p53 DNA binding and total p53 level in human thyroid cancer cell line ARO." Diss., Online access via UMI:, 2007.

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22

Huang, Shirley Chien-Chieh 1978. "Control of tumor suppressor p53 by protein phosphorylation and ER stress." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78384.

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Tumor suppressor p53 is a mediator of stress-induced cell cycle arrest and apoptosis. The kinase inhibitor 2-aminopurine (2-AP) is an adenine analog shown to cause cells to bypass DNA damage-induced cellular arrest through unknown mechanisms, and may potentially target p53. Although p53 plays vital roles in adaptation to many stresses, its role in cellular response to endoplasmic reticulum (ER) stress is unclear. Here, stress-induced p53 stabilization and checkpoint control in the presence of 2-AP are examined, as well as p53 regulation upon ER stress induction. I show that 2-aminopurin

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23

Zhang, Yuan. "An investigation of p53’s differential activation of cell cycle arrest and apoptosis." Thesis, Curtin University, 2008. http://hdl.handle.net/20.500.11937/1577.

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The p53 tumour suppressor protein lies at the hub of a very complex network of cellular pathways including apoptosis, cell cycle arrest, DNA repair and cellular senescence. However, the mechanism of why and how p53 switches between apoptosis and cell cycle arrest, thereby determining a cell’s fate, remains a mystery to us. To enable us to investigate this ability of p53 to switch between cell cycle arrest and apoptosis, we developed a model which demonstrates similar p53 expression patterns but different functional outcomes. Treating cells with Cisplatin (a common chemotherapeutic drug) and Nu

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24

Worrall, Erin G. "Novel concepts in MDM2 protein regulation." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3889.

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The tumour suppressor p53 has evolved a MDM2-dependent feedback loop that has a dual role as either a stimulator of p53 protein translation through mRNA binding or a stimulator of p53 protein degradation through the ubiquitin-proteasome system. A unique pseudo-substrate motif or “lid” in MDM2 is adjacent to its N-terminal hydrophobic drug-binding pocket and we have evaluated whether the lid of MDM2 is a physiological regulator of this dual function of MDM2. Deletion of this flexible pseudosubstrate motif inhibits MDM2 indicating that this peptide stretch can function as a positive regulatory m

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25

Rahman-Roblick, Rubaiyat. "The P53 pathway: role of telomerase and identification of novel targets : acts of a master regulator of tumor suppression /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-184-5/.

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26

Kulikov, Roman. "Regulation of the p53 tumor suppressor protein by glycogen synthase kinase 3." Karlsruhe : FZKA, 2005. http://bibliothek.fzk.de/zb/berichte/FZKA7124.pdf.

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27

Pääjärvi, Gerd. "Xenobiotics-induced phosphorylations of MDM2 /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-951-3/.

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28

Kovi, Ramesh C. "Defining the Role of CtBP2 in p53-Independent Tumor Suppressor Function of ARF: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/433.

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ARF, a potent tumor suppressor, positively regulates p53 by antagonizing MDM2, a negative regulator of p53, which in turn, results in either apoptosis or cell cycle arrest. ARF also suppresses the proliferation of cells lacking p53, and loss of ARF in p53-null mice, compared with ARF-null or p53-null mice, results in a broadened tumor spectrum and decreased tumor latency. This evidence suggests that ARF exerts both p53-dependent and p53-independent tumor suppressor activity. However, the molecular pathway and mechanism of ARF’s p53-independent tumor suppressor activity is not understood. The a

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29

Zhang, Yuan. "An investigation of p53’s differential activation of cell cycle arrest and apoptosis." Curtin University of Technology, School of Pharmacy, 2008. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=118347.

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The p53 tumour suppressor protein lies at the hub of a very complex network of cellular pathways including apoptosis, cell cycle arrest, DNA repair and cellular senescence. However, the mechanism of why and how p53 switches between apoptosis and cell cycle arrest, thereby determining a cell’s fate, remains a mystery to us. To enable us to investigate this ability of p53 to switch between cell cycle arrest and apoptosis, we developed a model which demonstrates similar p53 expression patterns but different functional outcomes. Treating cells with Cisplatin (a common chemotherapeutic drug) and Nu

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30

Bertoni, Sara <1982&gt. "The balance between rRNA and ribosomal protein synthesis up-and down- regulates the tumour suppressor p53 in mammalian cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3378/.

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31

Maetens, Marion M. "Regulation of the tumor suppressor p53 by Mdm2 and Mdm4." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210602.

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Mdm2 and Mdm4 are critical negative regulators of the p53 tumor suppressor. Mdm4-null mutants are severely anemic and exhibit impaired proliferation of the fetal liver erythroid lineage cells. This phenotype may indicate a cell-intrinsic function of Mdm4 in erythropoiesis. In contrast, red blood cell count was nearly normal in mice engineered to express low levels of Mdm2, suggesting that Mdm2 might be dispensable for red cell production. In the first part of the thesis, we further explore the tissue-specific functions of Mdm2 and Mdm4 in the erythroid lineage by crossing the conditional Mdm4

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32

Qian, Yingjuan. "The role of DEC1 in P53-dependent cellular senescence." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/qian.pdf.

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33

Hinnis, Adel Rady. "The tumour suppressor P53 and apoptotic regulatory proteins in breast cancer survival and response to therapy." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29510.

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Many breast cancer patients receive chemotherapy as part of their treatment, but unlike hormonal therapy there are no specific markers for predicting response. Almost all cancer therapies induce cell death by apoptosis. Therefore, factors that control apoptosis such as the tumour suppressor p53 and other regulatory proteins could provide important clues.;Initially breast cell lines (MCF-7, T47-D, ZR-75, MDA-MB-231, MDA-MB-468, HBL-100 and MBA-MB-436) were characterised with regard to proliferation, apoptosis, p53 and phosphorylated p53, p21waf-1, ChK2, bcl-2, bax, bcl-x, survivin and XIAP, usi

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34

Shouse, Geoffrey P. "Characterization of the functional interaction between two tumor suppressors p53 and B56Gamma-PP2A /." Diss., UC access only, 2009. http://proquest.umi.com/pqdweb?index=31&did=1790085501&SrchMode=1&sid=2&Fmt=7&retrieveGroup=0&VType=PQD&VInst=PROD&RQT=309&VName=PQD&TS=1270138690&clientId=48051.

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35

Harms, Kelly Lynn. "Mechanisms of P53-mediated apoptosis." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/harms.pdf.

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36

Zache, Nicole. "Studies of mutant p53-targeting small molecules /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-322-1/.

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37

Daniels, Paula Rosamund. "Characterisation of HPV type 16 E6 interactions with p53 and E6-associated protein in vitro and ex vivo." Thesis, University of York, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387558.

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38

Dimitrio, Luna. "MODELLING NUCLEOCYTOPLASMIC TRANSPORT WITH APPLICATION TO THE INTRACELLULAR DYNAMICS OF THE TUMOR SUPPRESSOR PROTEIN P53." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00769901.

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In this thesis, I discuss two main subjects coming from biology and I propose two models that mimic the behaviours of the biological networks studied. The first part of the thesis deals with intracellular transport of molecules. Proteins, RNA and, generally, any kind of cargo molecules move freely in the cytoplasm: intracellular transport as a consequence of Brownian motion is classically modelled as a diffusion process. Some specific proteins, like the tumour suppressor p53, use microtubules to facilitate their way towards the nucleus. Microtubules are a dense network of filaments that point

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39

Ryk, Charlotta. "Influence of genetic polymorphisms on DNA repair, p53 mutations and cancer risk /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-940-8/.

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40

Boldrup, Linda. "p63 and potential p63 targets in squamous cell carcinoma of the head and neck." Doctoral thesis, Umeå : Univ, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1522.

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41

Carr, Michael I. "The Role of MDM2 Phosphorylation in P53 Responses to DNA Damage and Tumor Suppression: A Dissertation." eScholarship@UMMS, 2016. http://escholarship.umassmed.edu/gsbs_diss/847.

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The p53 tumor suppressor protein is upregulated in response to DNA damage and other stress signals. The upregulation of p53 involves freeing it from negative regulation imposed by Mdm2 and MdmX (Mdm4). Accumulating evidence indicates that phosphorylation of Mdm proteins by different stress-activated kinases such as ATM or c-Abl significantly impacts p53 functions. We have previously shown that ATM phosphorylation of Mdm2 Ser394 is required for robust p53 stabilization and activation following DNA damage. This dissertation describes in vivo examination of the mechanism by which Mdm2 Ser394 phos

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42

Awad, Keytam Salem. "Inhibition of human papilloma virus E6 oncogene function by mammalian lignans activates the p53 tumor suppressor protein and induces apoptosis in cervical cancer cells." [Kent, Ohio] : Kent State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1183405761.

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Thesis (Ph.D.)--Kent State University, 2007.<br>Title from PDF t.p. (viewed July 8, 2009). Advisor: Angelo L. DeLucia. Keywords: human papilloma virus, mammalian lignans, p53, E6 oncogene. Includes bibliographical references (p. 133-149).

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43

Ramasubramanian, Brinda. "Combinatorial Approaches to Study Protein Stability: Design and Application of Cell-Based Screens to Engineer Tumor Suppressor Proteins." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1325256130.

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44

Berger, François. "Étude et caractérisation de mécanismes suppresseurs dans les tumeurs cérébrales humaines et le cerveau non tumoral : anti-tyrosine kinase, p53 et ciblage exogène par le thymidine kinase herpétique." Université Joseph Fourier (Grenoble), 1995. http://www.theses.fr/1995GRE10109.

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Nous avons identifié dans les liquides kystiques des gliomes, un facteur de 17 KDA porteur d'une activité de type anti-tyrosine kinase. Ce facteur est présent dans le cerveau normal ainsi que dans les tissus tumoraux. Il pourrait réaliser un élément modulateur de la prolifération cellulaire des cellules sensibles a l'EGF, tumorales ou non, en particulier des cellules souches neuro-ectodermiques. Une hyperexpression de la protéine p53 est observée dans 45% des astrocytomes. La présence de cellules hyperexprimant une protéine p53 de conformation mutée est étroitement liée à la progression tumora

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45

Sagne, Charlotte. "Polymorphisms in G-quadruplex regions of the TP53 tumour suppressor gene : Impact on cancer susceptibility and expression of p53 N-terminal isoforms." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T072/document.

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Le gène TP53 est extrêmement polymorphique avec 85 polymorphismes décrits. Certains de ces polymorphismes sont associés à une augmentation du risque de cancer, par exemple rs10425222 peut moduler les fonctions de p53. Cependant, pour d’autres, comme le rs17878362 qui est le polymorphisme intronique le plus étudié, leur association avec une augmentation du riques au cancer est controversée.Pour analyser l’association entre le polymorphisme rs17878362 et la susceptibilité au cancer, nous avons analysé son rôle dans des contextes de cancers sporadiques et familiaux. Les résultats obtenus pour le

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46

OGDEN, STACEY KATHRYN. "HBx-MEDIATED DISRUPTION OF p53 TUMOR SUPPRESSOR PROTEIN FUNCTION LEADING TO RE-ACTIVATION OF A SILENCED TUMOR MARKER GENE." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1014751166.

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47

Helton, Eric Scott. "A role for p63 in the regulation of cell cycle progression and cell death." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. http://www.mhsl.uab.edu/dt/2007p/helton.pdf.

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48

Walls, Ken C. "Molecular characterization of neural apoptosis." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009p/walls.pdf.

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49

Marusyk, Andriy. "Decreased cellular fitness as a tumor promoter /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado at Denver and Health Sciences Center, 2006.<br>Typescript. Includes bibliographical references (leaves 124-145). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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50

Karafin, Teele. "Etude de la fonction de Translationally Controlled Tumor Protein (TCTP) dans différents modèles génétiques dans la souris." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS211.

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TCTP est une protéine de 20 kDa que l’on retrouve souvent sous forme de dimère. Elle est fortement conservée dans la phylogénie et on la trouve dans les levures, les plantes, les invertébrés et les mammifères. Elle est localisée dans tous les compartiments de la cellule : noyau, cytoplasme, et membranes. Il s’agit d’une protéine très abondante dans des cellules souches ainsi que des cellules en croissance exponentielle, y compris les cellules tumorales. Sa fonction principale est celle d’une « protéine de survie ». TCTP a été décrite comme interagissant avec de multiples protéines dont p53, MD

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