Relevant bibliographies by topics / Mutants de p53

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mutants de p53'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Mutants de p53"

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Wang, GuoZhen, and Alan R. Fersht. "Propagation of aggregated p53: Cross-reaction and coaggregation vs. seeding." Proceedings of the National Academy of Sciences 112, no. 8 (2015): 2443–48. http://dx.doi.org/10.1073/pnas.1500262112.

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Destabilized mutant p53s coaggregate with WT p53, p63, and p73 in cancer cell lines. We found that stoichiometric amounts of aggregation-prone mutants induced only small amounts of WT p53 to coaggregate, and preformed aggregates did not significantly seed the aggregation of bulk protein. Similarly, p53 mutants trapped only small amounts of p63 and p73 into their p53 aggregates. Tetrameric full-length protein aggregated at similar rates and kinetics to isolated core domains, but there was some induced aggregation of WT by mutants in hetero-tetramers. p53 aggregation thus differs from the usual
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Raycroft, L., J. R. Schmidt, K. Yoas, M. M. Hao, and G. Lozano. "Analysis of p53 mutants for transcriptional activity." Molecular and Cellular Biology 11, no. 12 (1991): 6067–74. http://dx.doi.org/10.1128/mcb.11.12.6067.

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The wild-type p53 protein functions to suppress transformation, but numerous mutant p53 proteins are transformation competent. To examine the role of p53 as a transcription factor, we made fusion proteins containing human or mouse p53 sequences fused to the DNA binding domain of a known transcription factor, GAL4. Human and mouse wild-type p53/GAL4 specifically transactivated expression of a chloramphenicol acetyltransferase reporter in HeLa, CHO, and NIH 3T3 cells. Several mutant p53 proteins, including a mouse p53 mutant which is temperature sensitive for suppression, were also analyzed. A p
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Raycroft, L., J. R. Schmidt, K. Yoas, M. M. Hao, and G. Lozano. "Analysis of p53 mutants for transcriptional activity." Molecular and Cellular Biology 11, no. 12 (1991): 6067–74. http://dx.doi.org/10.1128/mcb.11.12.6067-6074.1991.

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The wild-type p53 protein functions to suppress transformation, but numerous mutant p53 proteins are transformation competent. To examine the role of p53 as a transcription factor, we made fusion proteins containing human or mouse p53 sequences fused to the DNA binding domain of a known transcription factor, GAL4. Human and mouse wild-type p53/GAL4 specifically transactivated expression of a chloramphenicol acetyltransferase reporter in HeLa, CHO, and NIH 3T3 cells. Several mutant p53 proteins, including a mouse p53 mutant which is temperature sensitive for suppression, were also analyzed. A p
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Scian, Mariano J., Katherine E. R. Stagliano, Michelle A. E. Anderson та ін. "Tumor-Derived p53 Mutants Induce NF-κB2 Gene Expression". Molecular and Cellular Biology 25, № 22 (2005): 10097–110. http://dx.doi.org/10.1128/mcb.25.22.10097-10110.2005.

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ABSTRACT Overexpression of mutant p53 is a common theme in tumors, suggesting a selective pressure for p53 mutation in cancer development and progression. To determine how mutant p53 expression may lead to survival advantage in human cancer cells, we generated stable cell lines expressing p53 mutants p53-R175H, -R273H, and -D281G by use of p53-null human H1299 (lung carcinoma) cells. Compared to vector-transfected cells, H1299 cells expressing mutant p53 showed a survival advantage when treated with etoposide, a common chemotherapeutic agent; however, cells expressing the transactivation-defic
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Ohiro, Yoichi, Anny Usheva, Shinichiro Kobayashi, et al. "Inhibition of Stress-Inducible Kinase Pathways by Tumorigenic Mutant p53." Molecular and Cellular Biology 23, no. 1 (2003): 322–34. http://dx.doi.org/10.1128/mcb.23.1.322-334.2003.

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ABSTRACT More than 50% of human cancers contain p53 gene mutations and as a result accumulate altered forms of the full-length p53 protein. Although certain tumor types expressing mutant p53 protein have a poor prognostic process, the precise role of mutant p53 protein in highly malignant tumor cells is not well defined. Some p53 mutants, but not wild-type p53, are shown here to interact with Daxx, a Fas-binding protein that activates stress-inducible kinase pathways. Interaction of Daxx with p53 is highly dependent upon the specific mutation of p53. Tumorigenic mutants of p53 bind to Daxx and
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Hall, Callum, and Patricia A. J. Muller. "The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer." International Journal of Molecular Sciences 20, no. 24 (2019): 6188. http://dx.doi.org/10.3390/ijms20246188.

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The p53 family of proteins has grown substantially over the last 40 years. It started with p53, then p63, p73, isoforms and mutants of these proteins. The function of p53 as a tumour suppressor has been thoroughly investigated, but the functions of all isoforms and mutants and the interplay between them are still poorly understood. Mutant p53 proteins lose p53 function, display dominant-negative (DN) activity and display gain-of-function (GOF) to varying degrees. GOF was originally attributed to mutant p53′s inhibitory function over the p53 family members p63 and p73. It has become apparent th
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Rockwell, Nathan, Max Staller, Maria Cannella, Barak Cohen, and Joshua Rubin. "GENE-59. NOT ALL p53 MUTATIONS ARE CREATED EQUAL: A MURINE ASTROCYTE MODEL FOR HIGH-THROUGHPUT FUNCTIONAL ASSESSMENT OF p53 MISSENSE MUTATIONS." Neuro-Oncology 21, Supplement_6 (2019): vi110. http://dx.doi.org/10.1093/neuonc/noz175.461.

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Abstract The tumor suppressor TP53 (p53) is the most commonly mutated gene in cancer and among the most frequently mutated genes in glioblastoma (GBM). The majority of p53 mutations in GBM are missense mutations in the DNA binding domain that lead to the production of full length mutant p53 protein. In addition to the complete loss of tumor suppressor function, these mutations have gain-of-function (GOF) properties either through attenuation of wild-type function or neomorphic functions. The variability in GOF mutations results in heterogeneity in cancer phenotypes between mutants that remain
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Shaulian, E., A. Zauberman, D. Ginsberg, and M. Oren. "Identification of a minimal transforming domain of p53: negative dominance through abrogation of sequence-specific DNA binding." Molecular and Cellular Biology 12, no. 12 (1992): 5581–92. http://dx.doi.org/10.1128/mcb.12.12.5581.

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Mutations in the p53 gene are most frequent in cancer. Many p53 mutants possess transforming activity in vitro. In cells transformed by such mutants, the mutant protein is oligomerized with endogenous cell p53. To determine the relevance of oligomerization for transformation, miniproteins containing C-terminal portions of p53 were generated. These miniproteins, although carrying no point mutation, transformed at least as efficiently as full-length mutant p53. Transforming activity was coupled with the ability to oligomerize with wild-type p53, as well as with the ability to abrogate sequence-s
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Shaulian, E., A. Zauberman, D. Ginsberg, and M. Oren. "Identification of a minimal transforming domain of p53: negative dominance through abrogation of sequence-specific DNA binding." Molecular and Cellular Biology 12, no. 12 (1992): 5581–92. http://dx.doi.org/10.1128/mcb.12.12.5581-5592.1992.

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Mutations in the p53 gene are most frequent in cancer. Many p53 mutants possess transforming activity in vitro. In cells transformed by such mutants, the mutant protein is oligomerized with endogenous cell p53. To determine the relevance of oligomerization for transformation, miniproteins containing C-terminal portions of p53 were generated. These miniproteins, although carrying no point mutation, transformed at least as efficiently as full-length mutant p53. Transforming activity was coupled with the ability to oligomerize with wild-type p53, as well as with the ability to abrogate sequence-s
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Muller, Patricia A. J., Karen H. Vousden, and Jim C. Norman. "p53 and its mutants in tumor cell migration and invasion." Journal of Cell Biology 192, no. 2 (2011): 209–18. http://dx.doi.org/10.1083/jcb.201009059.

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In about half of all human cancers, the tumor suppressor p53 protein is either lost or mutated, frequently resulting in the expression of a transcriptionally inactive mutant p53 protein. Loss of p53 function is well known to influence cell cycle checkpoint controls and apoptosis. But it is now clear that p53 regulates other key stages of metastatic progression, such as cell migration and invasion. Moreover, recent data suggests that expression of mutant p53 is not the equivalent of p53 loss, and that mutant p53s can acquire new functions to drive cell migration, invasion, and metastasis, in pa
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Dissertations / Theses on the topic "Mutants de p53"

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Ang, H. C. "Biophysical characterisation and rescue of p53 cancer mutants." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596120.

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The aim of this thesis was to use biophysical methods to characterise the stabilities and DNA binding properties of monomeric and tetrameric p53 cancer mutants, and to study various approaches aimed at rescuing structural mutants of p53. A detailed study of the destabilising effects of p53 mutations was performed using differential scanning calorimetry and urea denaturation, while equilibrium binding of p53 mutants to a specific promoter sequence, <i>gadd45</i>, was studied using fluorescence anisotropy and analytical ultracentrifugation. This thesis will also discuss how p53 structural mutant
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Estevan, Barber Anna. "Influence of genotoxic drug-induced post-translational modifications on mutant p53 stability and oncogenic activities." Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/1ec28205-8590-4044-91b0-0c5f68206c2c.

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The tumour suppressor p53 is often disrupted by missense mutations that can result in p53 protein accumulation and acquisition of novel oncogenic activities. Various studies have demonstrated that DNA-damaging drugs currently used in the clinic aimed at activating wild type p53, can also stabilise and activate mutant p53 oncogenic functions and thereby paradoxically enhance tumour progression, resulting in poor response to the treatment. In this study we aimed to investigate whether, like in wt p53, post-translational modifications (PTMs) drive such drug-induced mutant p53 accumulation and act
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Souza, Felipe da Costa. "Geração e caracterização de linhagens isogênicas portadoras de mutantes de p53: modelo para avaliar a estratégia de reparação dos genes p53 e p16 INK4A na presença dos mutantes p53R175H e p53R248Q." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-26072012-102241/.

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A destruição funcional das vias de controle do ciclo celular constituem um evento comuns em todos os tumores humanos. Muitos estudos associam mutações em p53 com mau prognostico no tratamento do câncer. Nesse trabalho, visamos a geração e caracterização de linhagens isogênicas portando diferentes mutantes de p53 como modelo de estudo para remediação simultânea de p53 e p16 na presença de mutantes hotspots específicos. Os mutantes R175H e R248Q não geraram alterações na cinética de proliferação da linhagem H358, mas levaram a um aumento de 27,5% na eficiência de plaqueamento e, no caso de R248Q
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Roger, Lauréline. "Etude des mécanismes de la régulation de l'EMT par le suppresseur de tumeur p53 dans un modèle de cellules de carcinome du colon." Montpellier 2, 2007. http://www.theses.fr/2007MON20182.

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Le suppresseur de tumeur p53 est un facteur de transcription impliqué dans la progression du cycle cellulaire et dans l'apoptose. Outre ses fonctions majeures, p53 régule également la migration et l'adhérence cellulaire qui sont deux évènements impliqués dans le processus métastatique. L'évolution maligne d'un carcinome peut aussi impliquer la répression transcriptionnelle de CDH1, qui code pour la E-cadhérine, protéine constitutive des jonctions adhérentes. Nous avons recherché si et comment p53 régule certains évènements moléculaires qui contrôle le processus métastatique. Nous montrons que
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Li, Lianjie. "Mutations in tumor suppressor p53 and deregulation of cellular metabolism." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19513.

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Mutation des p53 Gen ist die häufigste genetische Veränderung in allen humanen Tumoren. Weit verbreitete p53 misssense-Mutationen heben die Tumor suppressive Funktion auf und führen zu gain-of-function Eigenschaften, die Tumorproliferation, Chemoresistenz, Angiogenese, Migration, Invasion und Metastasen fördern. In dieser Arbeit haben ich für drei solche Hotspot-Mutationen, p53R245Q, p53R246S und p53R270H, eine höhere Sensitivität gegenüber Behandlung mit Piperlongumine in p53-defizienten MEFs und Eµ-myc Lymphomzellen im Vergleich zur Kontrolle und den anderen drei Hotspot-Mutationen, p53R172
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Toppaldoddi, Katte Rao. "Role of rare calreticulin mutants and of the endoplasmic reticulum stress in the pathogenesis of myeloproliferative neoplasms." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC322/document.

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Après la découverte des mutations de la calréticuline dans les néoplasmes classiques myéloproliferatifs négatifs pour le Ph1, les travaux se sont focalisés sur les deux mutations les plus fréquentes, c'est-à-dire la calréticuline del52 et l’ins5, mais il existe environ 20% de mutants rares de la calréticuline (une cinquantaine), qui ont été classés en type-1 « like » et type-2 « like », classification basée sur leur structure. Cependant il reste à déterminer si cette classification est pertinente du point de vue fonctionnel, ce qui pourrait avoir des conséquences pour la prise en charge des pa
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Osadchuk, Olha. "Optimalizace izolace mutantního proteinu p53 a jeho DNA vazebné vlastnosti." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2020. http://www.nusl.cz/ntk/nusl-413550.

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Protein p53 je jednou z nejdůležitějších molekul v lidském těle. P53 reguluje celou řadu procesů v buňce, jako je například oprava DNA, buněčný cyklus nebo indukce apoptózy. Protein p53 je známý i jako „strážce genomu“. DNA vazebné schopnosti proteinu p53 jsou důležité pro normální vývoj a růst buňky. Mutace genu pro p53 mohou vést ke ztrátě jeho DNA vazebných vlastností a funkce nádorového supresoru, což muže způsobit rozvoj rakoviny. Teoretická část této diplomové práce je zaměřena na popis vlastností, funkce a mechanismus aktivace proteinu p53 a popis lokálních sekundárních struktur DNA. Hl
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Pellerano, Morgan. "Développement d'un biosenseur fluorescent d'un mutant de p53 sujet à l'agrégation dans les cancers." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT053.

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P53 est un suppresseur de tumeur qui joue un rôle clé dans la régulation de la transcription, la réparation de l'ADN, l'instabilité génétique, la sénescence, la régulation du cycle cellulaire et l'apoptose. Cette protéine, normalement nucléaire, se lie à l’ADN et régule la transactivation. Cependant, elle est souvent mutée dans les tumeurs humaines, entraînant une inactivation fonctionnelle et une prédisposition au cancer. Les mutants p53 se peuvent-être de deux catégories des mutants de « contact » ou « conformationnel ». Ces derniers entraînant des changements de conformation pouvant induire
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Saundh, Harpal. "Targeting mutant p53 in cSCCs." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/29e37f0d-5ed7-483c-9a92-87212934d72b.

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Cutaneous squamous cell carcinoma (cSCC) is a type of non-melanoma skin cancer that is the 4th most common cancer registration in Scotland after BCC, lung and breast cancer. Over 30,000 cSCC incidences are reported each year in the United Kingdom. In addition, around 1 in 4 skin cancer deaths in the UK are due to cSCCs. Amongst those highly prone to developing cSCCs include organ transplant recipient, immunosuppressed, recessive dystrophic epidermolysis bullosa (RDEB) and Xeroderma Pigmentosum (XP) patients. cSCC patients that display regional metastasis have a 5-year survival rate of 25-50%,
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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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Books on the topic "Mutants de p53"

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Deb, Swati Palit, and Sumitra Deb, eds. Mutant p53 and MDM2 in Cancer. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9211-0.

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Kuzniar, Beata. Human lymphoblastoid cell lines expressing mutant p53 exhibit decreased sensitivity to cisplatin-induced cytotoxicity. National Library of Canada, 1998.

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Haupt, Ygal, and Giovanni Blandino, eds. Human Tumor-Derived p53 Mutants: A Growing Family of Oncoproteins. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-961-7.

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Deb, Sumitra, and Swati Palit Deb. Mutant p53 and MDM2 in Cancer. Springer, 2016.

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Book chapters on the topic "Mutants de p53"

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Finlay, C. A., and R. S. Quartin. "Biological Phenotypes of Tumor-Derived Human p53 Mutants." In DNA Replication and the Cell Cycle. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77040-1_19.

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Kamada, Rui. "Quantitative Analysis for p53 Tetramerization Domain Mutants Reveals a Low Threshold for Tumor Suppressor Inactivation." In Springer Theses. Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54135-6_2.

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Monti, Olimpia, Alexander Damalas, Sabrina Strano, and Giovanni Blandino. "P73, P63 and Mutant P53: Members of Protein Complexs Floating in Cancer Cells." In 25 Years of p53 Research. Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-2922-6_10.

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Terzian, Tamara, and Guillermina Lozano. "Mutant p53-Driven Tumorigenesis." In p53 in the Clinics. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3676-8_5.

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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Wild-Type versus Mutant p53." In p53 Suppressor Gene. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_3.

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Shen, Jinfeng, Vladimir J. N. Bykov, and Klas G. Wiman. "Targeting Mutant p53 for Improved Cancer Therapy." In p53 in the Clinics. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3676-8_14.

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Joerger, Andreas C., Assaf Friedler, and Alan R. Fersht. "Wild Type p53 Conformation, Structural Consequences of p53 Mutations and Mechanisms of Mutant p53 Rescue." In 25 Years of p53 Research. Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-2922-6_17.

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Frum, Rebecca A., and Steven R. Grossman. "Mechanisms of Mutant p53 Stabilization in Cancer." In Subcellular Biochemistry. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9211-0_10.

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Santoro, Raffaela, Sabrina Strano, and Giovanni Blandino. "Transcriptional Regulation by Mutant p53 and Oncogenesis." In Subcellular Biochemistry. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9211-0_5.

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Yeudall, W. Andrew, Katharine H. Wrighton, and Sumitra Deb. "Mutant p53 in Cell Adhesion and Motility." In Methods in Molecular Biology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-236-0_11.

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Conference papers on the topic "Mutants de p53"

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Vidales, Karen Hernández, Edgar Guevara, Vanesa Olivares Illana, and Francisco Javier González. "Raman Spectroscopy of Wild Type and Mutants p53." In Latin America Optics and Photonics Conference. OSA, 2018. http://dx.doi.org/10.1364/laop.2018.tu3c.4.

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Wang, Haijin, Ruhui Shen, Haichao Wang, and Haohan Wang. "Active learning framework of informative p53 cancer rescue mutants." In 2017 Third International Conference on Advances in Electrical, Electronics, Information, Communication and Bio-Informatics (AEEICB). IEEE, 2017. http://dx.doi.org/10.1109/aeeicb.2017.7972384.

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Hernández Vidales, Karen, Edgar Guevara Codina, Vanesa Olivares Illana, and Francisco Javier González Contreras. "Multivariate analysis of Raman spectroscopy of wild type and mutants p53 cancer biomarker." In Imaging Spectrometry XXIII: Applications, Sensors, and Processing, edited by Emmett J. Ientilucci. SPIE, 2019. http://dx.doi.org/10.1117/12.2529411.

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Vilimas, Tomas, Keith Collins, Theresa Guerin, et al. "Abstract A17: p53 missense mutants R172H and R270H exhibit differential effects on tumorigenesis." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-a17.

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Yang, Lu. "Abstract 2487: disrupting binding of p53 mutants to PEPD unleashes their tumor suppressor activities." 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.am2021-2487.

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Rodriguez, Olga Catalina, Vamsi Kokula, Jason Catania, et al. "Abstract 4833: Glucose restriction induces degradation of p53 mutants via a selective autophagy-mediated pathway." 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.am10-4833.

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Yu, Xin, David Lubin, Sumana Narayanan, et al. "Abstract 2330: NSC319726 reactivates zinc-binding p53 mis-sense mutants using a novel dual mechanism." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2330.

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Huun, Johanna, Elisabet O. Berge, Johan R. Lillehaug, Per Eystein Lonning, and Stian Knappskog. "Abstract 3139: Identification and functional studies of p53 mutants detected in breast cancers after chemotherapy treatment." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3139.

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Yu, Valen Z., and Maria L. Lung. "Abstract 5462: Functional characterization of potential gain-of-function p53 mutants in esophageal squamous cell carcinoma." 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.am2018-5462.

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Flores, Brianna, and Elizabeth E. Hull. "Abstract 556: Oncogenic properties and response to HDAC inhibitor treatment of H1299 cells expressing GOF p53 mutants." 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.am2018-556.

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Reports on the topic "Mutants de p53"

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Hildegund, Ertl C. Vaccines to Breast Cancer Based on p53 Mutants. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada359979.

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Chen, Xiaoying. Restore Wild-Type Functions to P53 Mutants Using an RNA- Based Combinatorial Approach. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada353779.

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Green, Christopher. Restore Wild-Type Functions to P53 Mutants Using an RNA-Based Combinatorial Approach. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada392235.

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Murphy, Kristen, Renee O'Lear, and Jeffrey Rosen. Functional Significance of Mutant p53 in Breast Cancer. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada395615.

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O'Lear, Rene, and Jeffrey Rosen. Functional Significance of Mutant p53 in Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada409759.

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Prives, Carol. The Role of Mutant p53 Protein in Breast Cancer. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada300013.

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Prives, Carol L. The Role of Mutant p53 Protein in Breast Cancer. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada363399.

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Prives, Carol L. The Role of Mutant p53 Protein in Breast Cancer. Defense Technical Information Center, 1997. http://dx.doi.org/10.21236/ada344920.

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Liu, Gang. The Role of Mutant p53 in Progression of Prostate Cancer. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada483299.

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DeMasters, Gerald. Susceptibility to Radiation Induced Apoptosis and Senescence in p53 Wild Type and p53 Mutant Breast Tumor Cells. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada463568.

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