Littérature scientifique sur le sujet « Mutant p53 gain of function »
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Articles de revues sur le sujet "Mutant p53 gain of function"
Stein, Yan, Varda Rotter et Ronit Aloni-Grinstein. « Gain-of-Function Mutant p53 : All the Roads Lead to Tumorigenesis ». International Journal of Molecular Sciences 20, no 24 (8 décembre 2019) : 6197. http://dx.doi.org/10.3390/ijms20246197.
Texte intégralHall, Callum, et 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 (7 décembre 2019) : 6188. http://dx.doi.org/10.3390/ijms20246188.
Texte intégralChen, Sisi, Hao Yu, Michihiro Kobayashi, Rui Gao, H. Scott Boswell et Yan Liu. « Gain-of-Function Mutant p53 Enhances Hematopoietic Stem Cell Self-Renewal ». Blood 124, no 21 (6 décembre 2014) : 260. http://dx.doi.org/10.1182/blood.v124.21.260.260.
Texte intégralChiang, Yen-Ting, Yi-Chung Chien, Yu-Heng Lin, Hui-Hsuan Wu, Dung-Fang Lee et Yung-Luen Yu. « The Function of the Mutant p53-R175H in Cancer ». Cancers 13, no 16 (13 août 2021) : 4088. http://dx.doi.org/10.3390/cancers13164088.
Texte intégralOren, M., et V. Rotter. « Mutant p53 Gain-of-Function in Cancer ». Cold Spring Harbor Perspectives in Biology 2, no 2 (16 décembre 2009) : a001107. http://dx.doi.org/10.1101/cshperspect.a001107.
Texte intégralAschauer, Lydia, et Patricia A. J. Muller. « Novel targets and interaction partners of mutant p53 Gain-Of-Function ». Biochemical Society Transactions 44, no 2 (11 avril 2016) : 460–66. http://dx.doi.org/10.1042/bst20150261.
Texte intégralZhang, Yanhong, Wensheng Yan et Xinbin Chen. « Mutant p53 Disrupts MCF-10A Cell Polarity in Three-dimensional Culture via Epithelial-to-mesenchymal Transitions ». Journal of Biological Chemistry 286, no 18 (22 mars 2011) : 16218–28. http://dx.doi.org/10.1074/jbc.m110.214585.
Texte intégralZhang, Cen, Juan Liu, Dandan Xu, Tianliang Zhang, Wenwei Hu et Zhaohui Feng. « Gain-of-function mutant p53 in cancer progression and therapy ». Journal of Molecular Cell Biology 12, no 9 (28 juillet 2020) : 674–87. http://dx.doi.org/10.1093/jmcb/mjaa040.
Texte intégralCai, Bi-He, Zhi-Yu Bai, Ching-Feng Lien, Si-Jie Yu, Rui-Yu Lu, Ming-Han Wu, Wei-Chen Wu, Chia-Chi Chen et Yi-Chiang Hsu. « NAMPT Inhibitor and P73 Activator Represses P53 R175H Mutated HNSCC Cell Proliferation in a Synergistic Manner ». Biomolecules 12, no 3 (12 mars 2022) : 438. http://dx.doi.org/10.3390/biom12030438.
Texte intégralZhang, Ying, Feng Yuan, Cassandra Grello, Brian Reon, Myron Gibert, Collin Dube, Anindya Dutta, Eric Holland et Roger Abounader. « CSIG-07. GAIN-OF-FUNCTION MUTANT P53 REGULATES LONG-NONCODING RNAS IN GLIOBLASTOMA ». Neuro-Oncology 24, Supplement_7 (1 novembre 2022) : vii39—vii40. http://dx.doi.org/10.1093/neuonc/noac209.156.
Texte intégralThèses sur le sujet "Mutant p53 gain of function"
Vaughan, Catherine. « Investigation of Gain-of-Function Induced by Mutant p53 ». VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3965.
Texte intégralTurrell, Frances Kathryn. « Gain-of-function and dominant-negative effects of distinct p53 mutations in lung tumours ». Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271848.
Texte intégralHeath, Nikki. « An investigation into the role of microvesicles in mutant p53 invasive gain-of-function ». Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6895/.
Texte intégralScian, Mariano J. « MODULATION OF GENE EXPRESSION BY TUMOR-DERIVED MUTANT p53. ROLE OF TRANSACTIVATION IN GAIN-OF-FUNCTION ». VCU Scholars Compass, 2005. https://scholarscompass.vcu.edu/etd/5518.
Texte intégralWülfing, Verena [Verfasser], et Jochen [Akademischer Betreuer] Dahm-Daphi. « Stimulation of Homologous Recombination by P53 gain-of-function mutant M237I / Verena Wülfing. Betreuer : Jochen Dahm-Daphi ». Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1027574041/34.
Texte intégralNapoli, Marco. « A Pin1/mutant p53 axis promotes aggressiveness in breast cancer ». Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4602.
Texte intégralMutations in the TP53 gene are among the most frequent genetic alterations in human cancers. As a consequence of these mutations p53 loses its tumour suppressor functions and may acquire novel oncogenic activities (gain of function) sustaining tumour formation and progression. Many in vivo studies highlighted that mutant p53 gain of function is associated with elevated protein levels, supporting the notion that in tumour cells altered signalling could stabilize and activate mutant p53, with mechanisms similar to those required to stimulate wild-type p53. The aim of my PhD work was to investigate the mechanisms underlying mutant p53 gain of function, focusing on factors that might link cancer-related signalling with mutant p53 activity. An intriguing candidate for this role is the phosphorylationdependent prolyl isomerase Pin1, that transduces phosphorylation signalling into conformational changes affecting the functions of its substrates, as ours and other laboratories have reported for wild-type p53. Despite Pin1 supports wild-type p53 functions, Pin1 is frequently overexpressed in human tumours and has been shown to promote both Her2/Neu/Ras and Notch1 dependent transformation. So we reasoned that the physiological role of Pin1 as a component of checkpoint mechanisms might be subverted during tumourigenesis, thereby turning it into an essential partner of mutant p53 and a critical amplifier of its oncogenic functions. Indeed, we now demonstrate that Pin1 enhances tumourigenesis in a Li-Fraumeni mouse model and cooperates with mutant p53 in Ras-dependent cell transformation. In human breast cancer cells, Pin1 promotes both mutant p53 dependent inhibition of the anti-metastatic factor p63 and the induction of a mutant p53 transcriptional program to increase tumor aggressiveness. Accordingly, we have identified a transcriptional signature (the Pin1/mutant p53 signature) that is associated with poor prognosis in breast cancer and, in a cohort of patients, Pin1 over-expression influences the prognostic value of p53 mutation. Considering that TP53 mutation is more frequent in tumors with higher risk of recurrence such as triple-negative cases and that some of the Pin1/mutant p53 signature genes are over-expressed in triple negative breast cancers, our findings carry therapeutic implications for this kind of cancers and possibly also for other tumours bearing mutant p53 and high levels of Pin1.
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Masood, Rubana. « The Effects of Gain of Function Mutant p53 and p63 on EPS8 and CXCL5 Expression in Head and Neck Squamous Cell Carcinoma ». VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/530.
Texte intégralGadepalli, Venkat Sundar. « ISOLATION AND CHARACTERIZATION OF MULTIPOTENT LUNG STEM CELLS FROM p53 MUTANT MICE MODELS ». VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3644.
Texte intégralChollat-Namy, Marie. « Effet de l’inactivation du gène suppresseur de tumeur p53 et de sa réactivation pharmacologique sur la réponse cytotoxique anti-tumorale The Pharmalogical Reactivation of p53 Function Improves Breast Tumor Cell Lysis by Granzyme B and NK Cells Through Induction of Autophagy Mutant P53 Gain of Function Stimulates PD-L1 Expression ». Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL032.
Texte intégralImmune system plays an important role in the control and destruction of cancer cells. The major effectors of antitumor immune response are Natural Killer (NK) cells and the cytotoxic T lymphocytes, which recognize et destroy tumor cells by exocytosis of perforin and granzymes contained in cytotoxic granules. It has been previously shown in the laboratory that the tumor suppressor p53 plays an important role in this apoptotic pathway. However more than 50% of human tumors have p53 inactivating mutations which favor tumor development. Consequently, frequent p53 inactivation in human tumor could enable them to escape from destruction by cytotoxic immune cells. In this context, my thesis work has shown that the pharmacological reactivation of wild type p53 function in cancer cells expressing a mutated p53 increased their susceptibility to NK cell-mediated apoptosis cells through the induction of an autophagic process. Moreover, I tried to determine the link between p53 mutations and the expression of the immune checkpoint ligand PD-L1 which prevent efficient activation of cytotoxic cells and promote immune cells exhaustion. My work suggests that the expression of p53 mutants promotes an the expression of PD-L1 at the cancer cell surface. The study of the underlying mechanisms is still in progress
Choi, Sang H. « Study of p53 Gain of Function Mutations in p53-null Astrocytes ». VCU Scholars Compass, 2000. http://scholarscompass.vcu.edu/etd/4420.
Texte intégralChapitres de livres sur le sujet "Mutant p53 gain of function"
Blandino, Giovanni. « Gain-of-Function p53 ». Dans Encyclopedia of Cancer, 1–4. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2302-2.
Texte intégralBlandino, Giovanni. « Gain-of-Function p53 ». Dans Encyclopedia of Cancer, 1828–31. Berlin, Heidelberg : Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2302.
Texte intégralBlandino, Giovanni. « Gain of Function p53 ». Dans Encyclopedia of Cancer, 1486–89. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2302.
Texte intégralDas, Priyanka, Rajeev N. Bahuguna, Rohit Joshi, Sneh Lata Singla-Pareek et Ashwani Pareek. « In search of mutants for gene discovery and functional genomics for multiple stress tolerance in rice. » Dans Mutation breeding, genetic diversity and crop adaptation to climate change, 444–50. Wallingford : CABI, 2021. http://dx.doi.org/10.1079/9781789249095.0045.
Texte intégralRokudai, Susumu. « High-Throughput RNA Interference Screen Targeting Synthetic-Lethal Gain-of-Function of Oncogenic Mutant TP53 in Triple-Negative Breast Cancer ». Dans Methods in Molecular Biology, 297–303. New York, NY : Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0247-8_25.
Texte intégral« Oncogenomic Approaches in Exploring Gain of Function of Mutant p53 ». Dans Advances in Genome Science, sous la direction de Sara Donzelli, Francesca Biagioni, Francesca Fausti, Sabrina Strano, Giulia Fontemaggi et Giovanni Blandino, 143–60. BENTHAM SCIENCE PUBLISHERS, 2014. http://dx.doi.org/10.2174/9781608058204114030007.
Texte intégralAcikalin Coskun, Kubra, Merve Tutar, Mervenur Al, Asiye Gok Yurttas, Elif Cansu Abay, Nazlican Yurekli, Bercem Yeman Kiyak, Kezban Ucar Cifci et Yusuf Tutar. « Role of p53 in Human Cancers ». Dans P53 - A Guardian of the Genome and Beyond [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101961.
Texte intégralMcNamara, John M., et Olof Leimar. « Central Concepts ». Dans Game Theory in Biology, 13–26. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198815778.003.0002.
Texte intégralThompson, Gilbert R. « Familial hypercholesterolaemia ». Dans Oxford Textbook of Endocrinology and Diabetes, 1667–73. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1240.
Texte intégralMorales-Villegas, Enrique C., et Kausik K. Ray. « PCSK9 Inhibition with Evolocumab Reaching Physiologic LDL-C Levels for Reducing Atherosclerotic Burden and Cardiovascular Disease-The Full Landscape ». Dans Frontiers in Cardiovascular Drug Discovery : Volume 4, 148–85. BENTHAM SCIENCE PUBLISHERS, 2019. http://dx.doi.org/10.2174/9781681083995118040007.
Texte intégralActes de conférences sur le sujet "Mutant p53 gain of function"
Zhao, Yuhan, Cen Zhang, Xuetian Yue, Xiaoyan Li, Juan Liu, Haiyang Yu, Qifeng Yang, Zhaohui Feng et Wenwei Hu. « Abstract 1221 : Pontin, a new mutant p53 binding protein, promotes gain-of-function of mutant p53 ». Dans 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.am2015-1221.
Texte intégralLozano, Guillermina. « Abstract SY07-03 : Gain-of-function activities of mutant p53 ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-sy07-03.
Texte intégralLozano, Guillermina. « Abstract SY04-01 : The in vivo gain-of-function activities of mutant p53 ». Dans 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-sy04-01.
Texte intégralWei, Saisai, Sarah Malmut, Hongbo Wang et Chunhong Yan. « Abstract 788 : Effects of ATF3 on the gain-of-function of mutant p53. » Dans 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.am2013-788.
Texte intégralGuo, Xiaolan, Liyan Zhao, Hua Xiong, Kyle Auringer, Lei Wang et Yibin Deng. « Abstract 1173 : AKT-mTOR pathway mediates mutant p53 gain-of-function by inhibiting autophagy ». Dans Proceedings : AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012 ; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1173.
Texte intégralRedman-Rivera, Lindsay N., Timothy M. Shaver, Hailing Jin, Johanna M. Schafer, Quanhu Sheng, Rachel A. Hongo, Kathryn E. Beckermann, Brian D. Lehmann, Ferrin C. Wheeler et Jennifer A. Pietenpol. « Abstract 2489 : A functional genomics approach to determine mutant p53 gain-of-function mechanisms and phenotypes in tumorigenesis ». Dans 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.am2021-2489.
Texte intégralMartinez, Luis A., et Madhusudhan Kollareddy. « Abstract 2108 : Regulation of nucleotide metabolism by mutant p53 contributes to its gain-of-function activities ». Dans 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.am2015-2108.
Texte intégralJo, Se-Young, Hae-Min Moon, ChuHee Lee, Se Jin Jang et Young-Ah Suh. « Abstract A22 : Cell growth regulation of gain-of-function mutant p53 via miRNAs on metabolic inhibition ». Dans Abstracts : AACR Special Conference : Chromatin and Epigenetics in Cancer ; September 24-27, 2015 ; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-a22.
Texte intégralJo, Se-Young, Hye-Min Moon, ChuHee Lee, Se Jin Jang et Young-Ah Suh. « Abstract 2295 : AMP-activated protein kinase (AMPK) signaling in the context of gain-of-function mutant p53 in vivo ». Dans 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.am2015-2295.
Texte intégralBado, Igor, Fotis Nikolos, Gayani Rajapaksa, Jan-Ake Gustafsson et Christoforos Thomas. « Abstract 5043 : ERβ decreases the invasiveness of triple-negative breast cancer cells by regulating mutant p53 gain-of-function ». Dans 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.am2015-5043.
Texte intégralRapports d'organisations sur le sujet "Mutant p53 gain of function"
Shieh, Sheau-Yann, et Xinbin CHen. Function of Wild-type and Mutant Forms of p53 in Breast Cancer. Fort Belvoir, VA : Defense Technical Information Center, août 1997. http://dx.doi.org/10.21236/ada334430.
Texte intégralChamovitz, Daniel, et Albrecht Von Arnim. Translational regulation and light signal transduction in plants : the link between eIF3 and the COP9 signalosome. United States Department of Agriculture, novembre 2006. http://dx.doi.org/10.32747/2006.7696515.bard.
Texte intégralCasey, Therese, Sameer J. Mabjeesh, Avi Shamay et Karen Plaut. Photoperiod effects on milk production in goats : Are they mediated by the molecular clock in the mammary gland ? United States Department of Agriculture, janvier 2014. http://dx.doi.org/10.32747/2014.7598164.bard.
Texte intégralFromm, Hillel, Paul Michael Hasegawa et Aaron Fait. Calcium-regulated Transcription Factors Mediating Carbon Metabolism in Response to Drought. United States Department of Agriculture, juin 2013. http://dx.doi.org/10.32747/2013.7699847.bard.
Texte intégralMcClure, Michael A., Yitzhak Spiegel, David M. Bird, R. Salomon et R. H. C. Curtis. Functional Analysis of Root-Knot Nematode Surface Coat Proteins to Develop Rational Targets for Plantibodies. United States Department of Agriculture, octobre 2001. http://dx.doi.org/10.32747/2001.7575284.bard.
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