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Journal articles on the topic 'Mutants de p53'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

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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3

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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5

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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6

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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8

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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10

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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Gualberto, A., M. L. Hixon, T. S. Finco, N. D. Perkins, G. J. Nabel, and A. S. Baldwin. "A proliferative p53-responsive element mediates tumor necrosis factor alpha induction of the human immunodeficiency virus type 1 long terminal repeat." Molecular and Cellular Biology 15, no. 6 (1995): 3450–59. http://dx.doi.org/10.1128/mcb.15.6.3450.

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Transforming mutants of the p53 tumor suppressor gene can positively regulate transcription from several promoters that do not contain known p53 binding sites. Here, we report the identification of a novel p53 binding site in the human immunodeficiency virus long terminal repeat that specifically mediates mutant p53 transactivation. This DNA element was bound by endogenous Jurkat p53 when these cells were stimulated by tumor necrosis factor. Mutation of this sequence inhibited p53 transactivation and tumor necrosis factor inducibility of the human immunodeficiency virus type 1 long terminal re

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Barta, Julie A., Kristen Pauley, Andrew V. Kossenkov, and Steven B. McMahon. "The lung-enriched p53 mutants V157F and R158L/P regulate a gain of function transcriptome in lung cancer." Carcinogenesis 41, no. 1 (2019): 67–77. http://dx.doi.org/10.1093/carcin/bgz087.

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Abstract Lung cancer is the leading cause of cancer-related deaths in the USA, and alterations in the tumor suppressor gene TP53 are the most frequent somatic mutation among all histologic subtypes of lung cancer. Mutations in TP53 frequently result in a protein that exhibits not only loss of tumor suppressor capability but also oncogenic gain-of-function (GOF). The canonical p53 hotspot mutants R175H and R273H, for example, confer upon tumors a metastatic phenotype in murine models of mutant p53. To the best of our knowledge, GOF phenotypes of the less often studied V157, R158 and A159 mutant

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Merabet, Assia, Hellen Houlleberghs, Kate Maclagan, et al. "Mutants of the tumour suppressor p53 L1 loop as second-site suppressors for restoring DNA binding to oncogenic p53 mutations: structural and biochemical insights." Biochemical Journal 427, no. 2 (2010): 225–36. http://dx.doi.org/10.1042/bj20091888.

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To assess the potential of mutations from the L1 loop of the tumour suppressor p53 as second-site suppressors, the effect of H115N and S116M on the p53 ‘hot spot’ mutations has been investigated using the double-mutant approach. The effects of these two mutants on the p53 hot spots in terms of thermal stability and DNA binding were evaluated. The results show that: (i) the p53 mutants H115N and S116M are thermally more stable than wild-type p53; (ii) H115N but not S116M is capable of rescuing the DNA binding of one of the most frequent p53 mutants in cancer, R248Q, as shown by binding of R248Q

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Di Como, Charles J., Christian Gaiddon, and Carol Prives. "p73 Function Is Inhibited by Tumor-Derived p53 Mutants in Mammalian Cells." Molecular and Cellular Biology 19, no. 2 (1999): 1438–49. http://dx.doi.org/10.1128/mcb.19.2.1438.

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ABSTRACT The p53 tumor suppressor protein, found mutated in over 50% of all human tumors, is a sequence-specific transcriptional activator. Recent studies have identified a p53 relative, termed p73. We were interested in determining the relative abilities of wild-type and mutant forms of p53 and p73α and -β isoforms to transactivate various p53-responsive promoters. We show that both p73α and p73β activate the transcription of reporters containing a number of p53-responsive promoters in the p53-null cell line H1299. However, a number of significant differences were observed between p53 and p73

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Chan, Wan Mui, Wai Yi Siu, Anita Lau, and Randy Y. C. Poon. "How Many Mutant p53 Molecules Are Needed To Inactivate a Tetramer?" Molecular and Cellular Biology 24, no. 8 (2004): 3536–51. http://dx.doi.org/10.1128/mcb.24.8.3536-3551.2004.

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ABSTRACT The tumor suppressor p53 is transcription factor composed of four identical subunits. The majority of the mutations in p53 are missense mutations that impair DNA binding. On the other hand, the p53-related p63 and p73 genes are rarely mutated, but many cell types express natural variants lacking the N-terminal transactivation domain (NΔ). Compelling evidence indicates that both the DNA binding-defective and NΔ mutants can impair the function of wild-type p53 in a dominant-negative manner. Interestingly, it is uncertain how many mutant subunit(s) a p53 tetramer can tolerate. In this st

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Ludes-Meyers, J. H., M. A. Subler, C. V. Shivakumar, et al. "Transcriptional activation of the human epidermal growth factor receptor promoter by human p53." Molecular and Cellular Biology 16, no. 11 (1996): 6009–19. http://dx.doi.org/10.1128/mcb.16.11.6009.

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The human epidermal growth factor receptor (EGFR) promoter is activated by both wild-type and tumor-derived mutant p53. In this communication, we demonstrate that EGFR promoter sequence requirements for transactivation by wild-type and mutant p53 are different. Transient-expression assays with EGFR promoter deletions identified a wild-type human p53 response element, 5'-AGCTAGACGTCCGGGCAGCCCCCGGCG -3', from positions --265 to --239. Electrophoretic mobility shift analysis and DNase I footprinting assays indicated that wild-type p53 binds sequence specifically to the response element. Using cir

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Aurelio, Oscar N., Xiao-Tang Kong, Swati Gupta, and Eric J. Stanbridge. "p53 Mutants Have Selective Dominant-Negative Effects on Apoptosis but Not Growth Arrest in Human Cancer Cell Lines." Molecular and Cellular Biology 20, no. 3 (2000): 770–78. http://dx.doi.org/10.1128/mcb.20.3.770-778.2000.

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ABSTRACT A bidirectional expression vector that allowed equal transcription of cloned wild-type and mutant p53 cDNAs from the same vector was developed. The vector was transfected into CaLu 6 lung carcinoma cells or Saos-2 osteosarcoma cells. All p53 mutants examined were recessive to wild-type p53 transactivation ofp21WAF1/CIP1 but dominant-negative for transactivation of Bax. An examination of effects on growth arrest and apoptotic pathways indicated that all mutants were recessive to wild type for growth arrest but only three of seven mutants were dominant negative for induction of apoptosi

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De Souza, Cristabelle, Jill Madden, Devin C. Koestler, et al. "Effect of the p53 P72R Polymorphism on Mutant TP53 Allele Selection in Human Cancer." JNCI: Journal of the National Cancer Institute 113, no. 9 (2021): 1246–57. http://dx.doi.org/10.1093/jnci/djab019.

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Abstract Background TP53 mutations occur in more than 50% of cancers. We sought to determine the effect of the intragenic P72R single nucleotide polymorphism (SNP; rs1042522) on the oncogenic properties of mutant p53. Methods P72R allelic selection in tumors was determined from genotype calls and a Gaussian distributed mixture model. The SNP effect on mutant p53 was determined in p53-negative cancer cell lines. RNA-sequencing, chromatin immunoprecipitation, and survival analysis were performed to describe the SNP effect. All statistical tests were 2-sided. Results Among 409 patients with germl

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LeBrasseur, Nicole. "Big bones in p53 mutants." Journal of Cell Biology 172, no. 1 (2005): 2. http://dx.doi.org/10.1083/jcb1721iti2.

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Gummlich, Linda. "ATO stabilizes structural p53 mutants." Nature Reviews Cancer 21, no. 3 (2021): 141. http://dx.doi.org/10.1038/s41568-021-00337-1.

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Vasilevskaya, Irina, Jennifer McCann, Christopher McNair, Neermala Poudel Neupane, Peter Gallagher, and Karen E. Knudsen. "Significance of distinct specifically enriched missense TP53 mutations in prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (2020): 377. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.377.

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377 Background: The most common TP53 alterations are missense mutations occurring in the DNA binding domain. The majority of missense p53 mutants (mut-p53) demonstrate oncogenic gain-of-function (GOF) abilities, irrespective of wild-type p53 presence, and thus contribute to a more aggressive disease. In prostate cancer (PCa), characterized by comparatively low overall mutational burden, TP53 is frequently mutated in both primary and advanced disease. Despite significant progress made in the field, detailed mechanisms of GOF in PCa remain undefined due to differing features of p53 mutants. Meth

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Paron, I., C. D’Ambrosio, A. Scaloni, et al. "A differential proteomic approach to identify proteins associated with thyroid cell transformation." Journal of Molecular Endocrinology 34, no. 1 (2005): 199–207. http://dx.doi.org/10.1677/jme.1.01618.

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Tumour suppressor p53 is a transcription factor essential for DNA damage checkpoints during cellular response to stress. Mutations in the p53 gene are the most common genetic alterations found in human tumours; most pathogenetic modifications are missense mutations that abolish the p53 DNA-binding function. In the same cell type, distinct p53 missense mutations may determine different phenotypes. The PC Cl3 cell line retains several markers of thyroid differentiation in vitro. Introduction of the V143A mutant p53 allele, which abolishes the p53 DNA-binding function, leads to loss of differenti

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Donninger, Howard, Anke Binder, Lothar Bohm, and M. Iqbal Parker. "Differential effects of novel tumour-derived p53 mutations on the transformation of NIH-3T3 cells." Biological Chemistry 389, no. 1 (2008): 57–67. http://dx.doi.org/10.1515/bc.2008.010.

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AbstractThe p53 tumour suppressor gene is frequently mutated in human tumours and different tumour-derived mutations have varying effects on cells. The effect of a novel tumour-derived p53 mutation and two recently described mutations from South African breast cancer patients on the growth rate, colony formation, cell cycle arrest after irradiation and response to chemotherapeutic drugs was investigated. None of the p53 mutations had any significant effect on the inherent growth rate of the cells; however, contact inhibition of growth in two of the mutants was lost. These same two mutants form

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Gaiddon, C., M. Lokshin, J. Ahn, T. Zhang, and C. Prives. "A Subset of Tumor-Derived Mutant Forms of p53 Down-Regulate p63 and p73 through a Direct Interaction with the p53 Core Domain." Molecular and Cellular Biology 21, no. 5 (2001): 1874–87. http://dx.doi.org/10.1128/mcb.21.5.1874-1887.2001.

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ABSTRACT The p53 protein is related by sequence homology and function to the products of two other genes, p63 and p73, that each encode several isoforms. We and others have discovered previously that certain tumor-derived mutants of p53 can associate and inhibit transcriptional activation by the α and β isoforms of p73. In this study we have extended these observations to show that in transfected cells a number of mutant p53 proteins could bind and down-regulate several isoforms not only of p73 (p73α, -β, -γ, and -δ) but also of p63 (p63α and -γ; ΔNp63α and -γ). Moreover, a correlation existed

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Odell, Adam F., Luke R. Odell, Jon M. Askham, Hiba Alogheli, Sreenivasan Ponnambalam, and Monica Hollstein. "A Novel p53 Mutant Found in Iatrogenic Urothelial Cancers Is Dysfunctional and Can Be Rescued by a Second-site Global Suppressor Mutation." Journal of Biological Chemistry 288, no. 23 (2013): 16704–14. http://dx.doi.org/10.1074/jbc.m112.443168.

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Exposure to herbal remedies containing the carcinogen aristolochic acid (AA) has been widespread in some regions of the world. Rare A→T TP53 mutations were recently discovered in AA-associated urothelial cancers. The near absence of these mutations among all other sequenced human tumors suggests that they could be biologically silent. There are no cell banks with established lines derived from human tumors with which to explore the influence of the novel mutants on p53 function and cellular behavior. To investigate their impact, we generated isogenic mutant clones by integrase-mediated cassett

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Vikhanskaya, F., M. K. Lee, M. Mazzoletti, M. Broggini, and K. Sabapathy. "Cancer-derived p53 mutants suppress p53-target gene expression--potential mechanism for gain of function of mutant p53." Nucleic Acids Research 35, no. 6 (2007): 2093–104. http://dx.doi.org/10.1093/nar/gkm099.

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Butera, Giovanna, Jessica Brandi, Chiara Cavallini, et al. "The Mutant p53-Driven Secretome Has Oncogenic Functions in Pancreatic Ductal Adenocarcinoma Cells." Biomolecules 10, no. 6 (2020): 884. http://dx.doi.org/10.3390/biom10060884.

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The cancer secretome is a rich repository of useful information for both cancer biology and clinical oncology. A better understanding of cancer secretome is particularly relevant for pancreatic ductal adenocarcinoma (PDAC), whose extremely high mortality rate is mainly due to early metastasis, resistance to conventional treatments, lack of recognizable symptoms, and assays for early detection. TP53 gene is a master transcriptional regulator controlling several key cellular pathways and it is mutated in ~75% of PDACs. We report the functional effect of the hot-spot p53 mutant isoforms R175H and

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Amelio, Ivano, Mara Mancini, Varvara Petrova, et al. "p53 mutants cooperate with HIF-1 in transcriptional regulation of extracellular matrix components to promote tumor progression." Proceedings of the National Academy of Sciences 115, no. 46 (2018): E10869—E10878. http://dx.doi.org/10.1073/pnas.1808314115.

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Mutations in the TP53 gene and microenvironmentally driven activation of hypoxia-inducible factor-1 (HIF-1) typically occur in later stages of tumorigenesis. An ongoing challenge is the identification of molecular determinants of advanced cancer pathogenesis to design alternative last-line therapeutic options. Here, we report that p53 mutants influence the tumor microenvironment by cooperating with HIF-1 to promote cancer progression. We demonstrate that in non-small cell lung cancer (NSCLC), p53 mutants exert a gain-of-function (GOF) effect on HIF-1, thus regulating a selective gene expressio

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Whitesell, Luke, Patrick D. Sutphin, Elizabeth J. Pulcini, Jesse D. Martinez, and Paul H. Cook. "The Physical Association of Multiple Molecular Chaperone Proteins with Mutant p53 Is Altered by Geldanamycin, an hsp90-Binding Agent." Molecular and Cellular Biology 18, no. 3 (1998): 1517–24. http://dx.doi.org/10.1128/mcb.18.3.1517.

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ABSTRACT Wild-type p53 is a short-lived protein which turns over very rapidly via selective proteolysis in the ubiquitin-proteasome pathway. Most p53 mutations, however, encode for protein products which display markedly increased intracellular levels and are associated with positive tumor-promoting activity. The mechanism by which mutation leads to impairment of ubiquitination and proteasome-mediated degradation is unknown, but it has been noted that many transforming p53 mutants are found in stable physical association with molecular chaperones of the hsp70 class. To explore a possible role

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Milner, J., E. A. Medcalf, and A. C. Cook. "Tumor suppressor p53: analysis of wild-type and mutant p53 complexes." Molecular and Cellular Biology 11, no. 1 (1991): 12–19. http://dx.doi.org/10.1128/mcb.11.1.12.

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It has been suggested that the dominant effect of mutant p53 on tumor progression may reflect the mutant protein binding to wild-type p53, with inactivation of suppressor function. To date, evidence for wild-type/mutant p53 complexes involves p53 from different species. To investigate wild-type/mutant p53 complexes in relation to natural tumor progression, we sought to identify intraspecific complexes, using murine p53. The mutant phenotype p53-246(0) was used because this phenotype is immunologically distinct from wild-type p53-246+ and thus permits immunological analysis for wild-type/mutant

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Milner, J., E. A. Medcalf, and A. C. Cook. "Tumor suppressor p53: analysis of wild-type and mutant p53 complexes." Molecular and Cellular Biology 11, no. 1 (1991): 12–19. http://dx.doi.org/10.1128/mcb.11.1.12-19.1991.

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It has been suggested that the dominant effect of mutant p53 on tumor progression may reflect the mutant protein binding to wild-type p53, with inactivation of suppressor function. To date, evidence for wild-type/mutant p53 complexes involves p53 from different species. To investigate wild-type/mutant p53 complexes in relation to natural tumor progression, we sought to identify intraspecific complexes, using murine p53. The mutant phenotype p53-246(0) was used because this phenotype is immunologically distinct from wild-type p53-246+ and thus permits immunological analysis for wild-type/mutant

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Shetty, Gunapala, Shan H. Shao, and Connie C. Y. Weng. "p53-Dependent Apoptosis in the Inhibition of Spermatogonial Differentiation in Juvenile Spermatogonial Depletion (Utp14bjsd) Mice." Endocrinology 149, no. 6 (2008): 2773–81. http://dx.doi.org/10.1210/en.2007-1338.

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In adult male mice homozygous for the juvenile spermatogonial depletion (Utp14bjsd) mutation in the Utp14b gene, type A spermatogonia proliferate, but in the presence of testosterone and at scrotal temperatures, these spermatogonia undergo apoptosis just before differentiation. In an attempt to delineate this apoptotic pathway in jsd mice and specifically address the roles of p53- and Fas ligand (FasL) /Fas receptor-mediated apoptosis, we produced jsd mice deficient in p53, Fas, or FasL. Already at the age of 5 wk, less degeneration of spermatogenesis was observed in p53-null-jsd mice than jsd

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Liu, Yun, Jason J. Chen, Qingshen Gao, et al. "Multiple Functions of Human Papillomavirus Type 16 E6 Contribute to the Immortalization of Mammary Epithelial Cells." Journal of Virology 73, no. 9 (1999): 7297–307. http://dx.doi.org/10.1128/jvi.73.9.7297-7307.1999.

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ABSTRACT The E6 proteins from cervical cancer-associated human papillomavirus (HPV) types such as HPV type 16 (HPV-16) induce proteolysis of the p53 tumor suppressor protein through interaction with E6-AP. We have previously shown that human mammary epithelial cells (MECs) immortalized by HPV-16 E6 display low levels of p53. HPV-16 E6 as well as other cancer-related papillomavirus E6 proteins also binds the cellular protein E6BP (ERC-55). To explore the potential functional significance of these interactions, we created and analyzed a series of E6 mutants for their ability to interact with E6-

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Ludwig, R. L., S. Bates, and K. H. Vousden. "Differential activation of target cellular promoters by p53 mutants with impaired apoptotic function." Molecular and Cellular Biology 16, no. 9 (1996): 4952–60. http://dx.doi.org/10.1128/mcb.16.9.4952.

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The p53 tumor suppressor protein is a sequence-specific transcriptional activator, a function which contributes to cell cycle arrest and apoptosis induced by p53 in appropriate cell types. Analysis of a series of p53 point mutants has revealed the potential for selective loss of the ability to transactivate some, but not all, cellular p53-responsive promoters. p53 175P and p53 181L are tumor-derived p53 point mutants which were previously characterized as transcriptionally active. Both mutants retained the ability to activate expression of the cyclin-dependent kinase inhibitor p2lcip1/waf1, an

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Babikir, Husam, Rayhaneh Afjei, Ramasamy Paulmurugan, and Tarik Massoud. "EXTH-30. PRECEDING p53 STABILIZATION USING DOXORUBICIN AUGMENTS PRIMA-1-MEDIATED p53 REFOLDING AND INCREASED CELLULAR APOPTOSIS: EVALUATION OF A SEQUENTIAL COMBINATION THERAPY AGAINST GLIOBLASTOMA." Neuro-Oncology 21, Supplement_6 (2019): vi88. http://dx.doi.org/10.1093/neuonc/noz175.362.

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Abstract INTRODUCTION Mutant p53 cancer cells are poorly responsive to chemotherapy. A small molecule drug, PRIMA-1, can bind to wildtype and mutant p53 to induce structural conformation that enhances p53 DNA binding. In a quest for new effective combination chemotherapies, we hypothesized that sequential treatment of GBM cells with doxorubicin then PRIMA-1 could stabilize and refold p53 to enhance chemotherapy-induced cellular apoptosis. We evaluated this combination in GBM cells engineered to express different p53 mutants and exhibiting different phenotypes. METHODS We constructed split repo

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Kamada, Rui, Takao Nomura, Carl W. Anderson, and Kazuyasu Sakaguchi. "Cancer-associated p53 Tetramerization Domain Mutants." Journal of Biological Chemistry 286, no. 1 (2010): 252–58. http://dx.doi.org/10.1074/jbc.m110.174698.

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Pochampally, Radhika, Changgong Li, Wenge Lu, et al. "Temperature-Sensitive Mutants of p53 Homologs." Biochemical and Biophysical Research Communications 279, no. 3 (2000): 1001–10. http://dx.doi.org/10.1006/bbrc.2000.4056.

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Sobhani, Navid, Alberto D’Angelo, Xu Wang, Ken H. Young, Daniele Generali, and Yong Li. "Mutant p53 as an Antigen in Cancer Immunotherapy." International Journal of Molecular Sciences 21, no. 11 (2020): 4087. http://dx.doi.org/10.3390/ijms21114087.

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The p53 tumor suppressor plays a pivotal role in cancer and infectious disease. Many oncology treatments are now calling on immunotherapy approaches, and scores of studies have investigated the role of p53 antibodies in cancer diagnosis and therapy. This review summarizes the current knowledge from the preliminary evidence that suggests a potential role of p53 as an antigen in the adaptive immune response and as a key monitor of the innate immune system, thereby speculating on the idea that mutant p53 antigens serve as a druggable targets in immunotherapy. Except in a few cases, the vast major

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Shivakumar, C. V., D. R. Brown, S. Deb, and S. P. Deb. "Wild-type human p53 transactivates the human proliferating cell nuclear antigen promoter." Molecular and Cellular Biology 15, no. 12 (1995): 6785–93. http://dx.doi.org/10.1128/mcb.15.12.6785.

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The wild-type p53 protein is a transcriptional activator implicated in the control of cellular growth-related gene expression. Here, using a number of different cell lines and transient-transfection-transcription assays, we demonstrate that at low levels, wild-type p53 transactivates the human proliferating cell nuclear antigen (PCNA) promoter. When expressed at a similar level, the tumor-derived p53 mutants did not transactivate the PCNA promoter. We identified a p53-binding site on the human PCNA promoter with which p53 interacts sequence specifically. When placed on a heterologous synthetic

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Hann, Byron, and Allan Balmain. "Replication of an E1B 55-Kilodalton Protein-Deficient Adenovirus (ONYX-015) Is Restored by Gain-of-Function Rather than Loss-of-Function p53 Mutants." Journal of Virology 77, no. 21 (2003): 11588–95. http://dx.doi.org/10.1128/jvi.77.21.11588-11595.2003.

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ABSTRACT ONYX-015 (dl1520) is an E1B 55-kilodalton protein-deficient replicating adenovirus that is currently in clinical trials as an antitumor agent. On the basis of the observation that the E1B 55kD gene product is able to bind to and inactivate p53, ONYX-015's mechanism of action is proposed to involve selective replication in and killing of p53-deficient cells. While its efficacy as a therapeutic agent appears evident, the virus's mechanism of cellular selectivity, including a possible role of p53 in this regard, is less clear. Indeed, there have been a number of recent reports suggesting

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Brosh, Ran, and Varda Rotter. "When mutants gain new powers: news from the mutant p53 field." Nature Reviews Cancer 9, no. 10 (2009): 701–13. http://dx.doi.org/10.1038/nrc2693.

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Candelaria, Nicholes, Achuth Padmanabhan, Rainer Lanz, Kwong Wong, and JoAnne S. Richards. "P53 Gain-of-Function Mutants and Steroids in Ovarian Cancer Cell Metastasis." Journal of the Endocrine Society 5, Supplement_1 (2021): A770—A771. http://dx.doi.org/10.1210/jendso/bvab048.1567.

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Abstract High-grade serous ovarian cancer (HGSOC) is a heterogeneous disease for which there currentlyis no cure. Because p53 is mutated in &gt;90% of all ovarian cancer, we studied specific gain-of-function (GOF) p53 mutants and steroid hormones for tumor morphology and metastasis in vivo. For this, we analyzed ALST (WT p53), SKOV3 (p53 null), TYK-NU (p53-R175H), OVCAR3 (p53-R248Q) and OVCA420 (p53-R273H) cell line xenografts in Foxn1-/- mice. ALST cells failed tometastasize, likely due to the known apoptotic effects of WT p53. SKOV3 and the p53-GOF celllines metastasized to the omentum a

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Pospisilova, Sarka, Jitka Malcikova, Jiri Damborsky, et al. "Role of p53 Gene Mutation Type in B-CLL Prognosis." Blood 108, no. 11 (2006): 4324. http://dx.doi.org/10.1182/blood.v108.11.4324.4324.

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Abstract Tumor suppressor p53 is a powerful transcription factor responsible for cell cycle regulation, which can bind about 300 different promoter elements in the human genome. Disruption of p53 function by mutation or deletion belongs to the most frequent alterations observed in human cancers, in B-CLL ranging from 10 to 15%. In our cohort of 230 B-CLL patients, we detected 10.5% patients with Tp53 mutation, 67% of these exhibited a point mutation (single nucleotide switch) largely combined with deletion of the second allele. The detected mutations are mostly localized in the DNA binding dom

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Wallentine, Brad D., Ying Wang, Vira Tretyachenko-Ladokhina, Martha Tan, Donald F. Senear, and Hartmut Luecke. "Structures of oncogenic, suppressor and rescued p53 core-domain variants: mechanisms of mutant p53 rescue." Acta Crystallographica Section D Biological Crystallography 69, no. 10 (2013): 2146–56. http://dx.doi.org/10.1107/s0907444913020830.

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To gain insights into the mechanisms by which certain second-site suppressor mutations rescue the function of a significant number of cancer mutations of the tumor suppressor protein p53, X-ray crystallographic structures of four p53 core-domain variants were determined. These include an oncogenic mutant, V157F, two single-site suppressor mutants, N235K and N239Y, and the rescued cancer mutant V157F/N235K/N239Y. The V157F mutation substitutes a smaller hydrophobic valine with a larger hydrophobic phenylalanine within strand S4 of the hydrophobic core. The structure of this cancer mutant shows

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Li, Hui, Jinglin Zhang, Joanna Hung Man Tong, et al. "Targeting the Oncogenic p53 Mutants in Colorectal Cancer and Other Solid Tumors." International Journal of Molecular Sciences 20, no. 23 (2019): 5999. http://dx.doi.org/10.3390/ijms20235999.

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Colorectal cancer (CRC) is a kind of solid tumor and the third most common cancer type in the world. It is a heterogeneous disease characterized by genetic and epigenetic aberrations. The TP53 mutation is the key step driving the transition from adenoma to adenocarcinoma. The functional roles of TP53 mutation in tumor development have been comprehensively investigated. In CRC, TP53 mutation was associated with poor prognosis and chemoresistance. A gain of function (GOF) of p53 mutants promotes cell proliferation, migration and invasion through multiple mechanisms. Restoring wild type p53 funct

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Fukumoto, Kota, Mamiko Sakata-Yanagimoto, Manabu Fujisawa, et al. "VAV1 Mutations Contributes to the Development of T-Cell Malignancies in Mice." Blood 134, Supplement_1 (2019): 300. http://dx.doi.org/10.1182/blood-2019-124591.

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Background: VAV1 is known as an important mediator of T-cell receptor (TCR) signaling through its guanine exchange factor (GEF)-dependent and independent functions. Recent studies identified activating VAV1 mutations in several types of T-cell malignancies including peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALCL), and adult T-cell lymphoma/leukemia (ATLL). However, the functions of VAV1 mutations in T-cell malignancies have not been clarified. Objective: We aim to identify the oncogeni

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De Souza, Cristabelle, Jill A. Madden, Dennis Minn, et al. "The P72R Polymorphism in R248Q/W p53 Mutants Modifies the Mutant Effect on Epithelial to Mesenchymal Transition Phenotype and Cell Invasion via CXCL1 Expression." International Journal of Molecular Sciences 21, no. 21 (2020): 8025. http://dx.doi.org/10.3390/ijms21218025.

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High-grade serous carcinoma (HGSC), the most lethal subtype of epithelial ovarian cancer (EOC), is characterized by widespread TP53 mutations (>90%), most of which are missense mutations (>70%). The objective of this study was to investigate differential transcriptional targets affected by a common germline P72R SNP (rs1042522) in two p53 hotspot mutants, R248Q and R248W, and identify the mechanism through which the P72R SNP affects the neomorphic properties of these mutants. Using isogenic cell line models, transcriptomic analysis, xenografts, and patient data, we found that the P72R SN

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ZHANG, Xian, Roger J. A. GRAND, Christopher J. McCABE, Jayne A. FRANKLYN, Phillip H. GALLIMORE та Andrew S. TURNELL. "Transcriptional regulation of the human glycoprotein hormone common α subunit gene by cAMP-response-element-binding protein (CREB)-binding protein (CBP)/p300 and p53". Biochemical Journal 368, № 1 (2002): 191–201. http://dx.doi.org/10.1042/bj20020634.

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We have investigated the functional interactions between adenovirus early region 1A (AdE1A) protein, the co-activators cAMP-response-element-binding protein (CREB)-binding protein (CBP)/p300 and SUG1, and the transcriptional repressor retinoblastoma (Rb) in mediating T3-dependent repression. Utilizing the human glycoprotein hormone common α-subunit (α-subunit) promoter and AdE1A mutants with selective binding capacity to these molecules we have determined an essential role for CBP/p300. In normal circumstances, wild-type 12S AdE1A inhibited α-subunit activity. In contrast, adenovirus mutants t

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Sidi, Samuel, Andreas T. Hagen, Richard Kennedy, et al. "Modifier Genetics in Zebrafish Identify Chk1 and an Associated Survival Pathway as Targets for Pharmacotherapy of MDS/AML with P53 Mutations." Blood 108, no. 11 (2006): 1432. http://dx.doi.org/10.1182/blood.v108.11.1432.1432.

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Abstract P53 mutations are frequently detected in high-risk MDS and AML cases with complex aberrant karyotypes (~20% of de novo MDS and AML cases). Pro-apoptotic signaling is a predominant mechanism through which wild-type p53 suppresses malignant transformation, and defects in this process account for the chemo/radio-resistance of many human tumors. The ability to sensitize p53 mutant myeloid cells to undergo apoptosis after drug or radiation therapy could accelerate the development of novel therapies for MDS, AML and other malignancies with p53 mutations. We have engineered a p53 mutant zebr

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Billant, Olivier, Gaëlle Friocourt, Pierre Roux, and Cécile Voisset. "p53, A Victim of the Prion Fashion." Cancers 13, no. 2 (2021): 269. http://dx.doi.org/10.3390/cancers13020269.

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Identified in the late 1970s as an oncogene, a driving force leading to tumor development, p53 turned out to be a key tumor suppressor gene. Now p53 is considered a master gene regulating the transcription of over 3000 target genes and controlling a remarkable number of cellular functions. The elevated prevalence of p53 mutations in human cancers has led to a recurring questioning about the roles of mutant p53 proteins and their functional consequences. Both mutants and isoforms of p53 have been attributed dominant-negative and gain of function properties among which is the ability to form amy

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