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P53 p63 p73 cancer

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https://www.readbyqxmd.com/read/28697449/binding-kinetics-of-mutant-p53r175h-with-wild-type-p53-and-p63-a-surface-plasmon-resonance-and-atomic-force-spectroscopy-study
#1
Ilaria Moscetti, Anna Rita Bizzarri, Salvatore Cannistraro
The oncogenic mutant p53R175H, one of the most frequently occurring in human cancers and usually associated with poor prognosis and chemo resistance, can exert a dominant negative effect over p53 family members, namely wild type p53, p63 and p73, inhibiting their oncosuppressive function. Novel anticancer strategies based on drugs able to prevent the formation of complexes between p53R175H and the p53 family members call for a deeper knowledge on the molecular mechanisms of their interaction. To this aim, p53R175H/p63 and p53R175H/p53 complexes were investigated in vitro by using Surface Plasmon Resonance and Atomic Force Spectroscopy, two emerging and complementary techniques able to provide interaction kinetic information, in near physiological conditions and without any labelling...
July 5, 2017: Biophysical Chemistry
https://www.readbyqxmd.com/read/28690024/the-p53-gene-with-emphasis-on-its-paralogues-in-mosquitoes
#2
REVIEW
Tien-Huang Chen, Yi-Jun Wu, Jiun-Nan Hou, Cheng-Hsun Chiu, Wei-June Chen
The p53 gene is highly important in human cancers, as it serves as a tumor-suppressor gene. Subsequently, two p53 homologues, i.e., p73 and p63, with high identity of amino acids were identified, leading to construction of the p53 family. The p53 gene is highly important in human cancer because it usually transcribes genes that function by causing apoptosis in mammalian cells. In contrast, p63 and p73 tend to be more important in modulating development than inducing cell death, even though they share similar protein structures...
June 29, 2017: Journal of Microbiology, Immunology, and Infection, Wei Mian Yu Gan Ran za Zhi
https://www.readbyqxmd.com/read/28654906/p53-p63-and-p73-in-the-wonderland-of-s-cerevisiae
#3
REVIEW
Olivier Billant, Marc Blondel, Cécile Voisset
Since its discovery in 1979, p53 has been on the forefront of cancer research. It is considered a master gene of cancer suppression and is found mutated in around 50% of all human tumors. In addition, the progressive identification of p53-related transcription factors p63 and p73 as well as their multiple isoforms have added further layers of complexity to an already dense network. Among the numerous models used to unravel the p53 family mysteries, S. cerevisiae has been particularly useful. This seemingly naive model allows the expression of a functional human p53 and thus the assessment of p53 intrinsic transcriptional activity...
June 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28635633/new-insights-in-thyroid-cancer-and-p53-family-proteins
#4
REVIEW
Livia Manzella, Stefania Stella, Maria Stella Pennisi, Elena Tirrò, Michele Massimino, Chiara Romano, Adriana Puma, Martina Tavarelli, Paolo Vigneri
Thyroid cancers are common endocrine malignancies that comprise tumors with different clinical and histological features. Indeed, papillary and follicular thyroid cancers are slow-growing, well-differentiated tumors, whereas anaplastic thyroid cancers are undifferentiated neoplasias that behave much more aggressively. Well-differentiated thyroid carcinomas are efficiently cured by surgery and radioiodine, unlike undifferentiated tumors that fail to uptake radioactive iodine and are usually resistant to chemotherapy...
June 21, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28526240/endocrine-actions-of-vitamin-d-in-skin-relevance-for-photocarcinogenesis-of-non-melanoma-skin-cancer-and-beyond
#5
REVIEW
Jörg Reichrath, Roman Saternus, Thomas Vogt
The skin represents a pivotal organ for the human body's vitamin D endocrine system, being both the site of ultraviolet (UV)-B-induced vitamin D synthesis and a target tissue for the pluripotent effects of 1,25(OH)2D3 and other biologically active vitamin D metabolites. As many other steroid hormones, 1,25(OH)2D3 exerts its effects via two independent signal transduction pathways: the classical genomic and the non-genomic pathway. While non-genomic effects of 1,25(OH)2D3 are in part exerted via effects on intracellular calcium, genomic effects are mediated by the vitamin D receptor (VDR)...
May 16, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28471195/-application-of-pla-method-for-detection-of-p53-p63-p73-complexes-in-situ-in-tumour-cells-and-tumour-tissue
#6
V Hrabal, M Nekulová, R Nenutil, J Holčaková, P J Coates, B Vojtěšek
BACKGROUND: PLA (proximity ligation assay) can be used for detection of protein-protein interactions in situ directly in cells and tissues. Due to its high sensitivity and specificity it is useful for detection, localization and quantification of protein complexes with single molecule resolution. One of the mechanisms of mutated p53 gain of function is formation of proten-protein complexes with other members of p53 family - p63 and p73. These interactions influences chemosensitivity and invasivity of cancer cells and this is why these complexes are potential targets of anti-cancer therapy...
2017: Klinická Onkologie: Casopis Ceské a Slovenské Onkologické Spolecnosti
https://www.readbyqxmd.com/read/28439015/mutant-p53-perturbs-dna-replication-checkpoint-control-through-topbp1-and-treslin
#7
Kang Liu, Fang-Tsyr Lin, Joshua D Graves, Yu-Ju Lee, Weei-Chin Lin
Accumulating evidence supports the gain-of-function of mutant forms of p53 (mutp53s). However, whether mutp53 directly perturbs the DNA replication checkpoint remains unclear. Previously, we have demonstrated that TopBP1 forms a complex with mutp53s and mediates their gain-of-function through NF-Y and p63/p73. Akt phosphorylates TopBP1 and induces its oligomerization, which inhibits its ATR-activating function. Here we show that various contact and conformational mutp53s bypass Akt to induce TopBP1 oligomerization and attenuate ATR checkpoint response during replication stress...
May 9, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28211873/the-p53-family-members-have-distinct-roles-during-mammalian-embryonic-development
#8
Jeanine L Van Nostrand, Margot E Bowen, Hannes Vogel, Maria Barna, Laura D Attardi
The p53 tumor suppressor is a member of a multi-protein family, including the p63 and p73 transcription factors. These proteins can bind to the same consensus sites in DNA and activate the same target genes, suggesting that there could be functional redundancy between them. Indeed, double mutant mice heterozygous for any two family member-encoding genes display enhanced cancer phenotypes relative to single heterozygous mutants. However, whether the family members play redundant roles during embryonic development has remained largely unexplored...
April 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27884017/the-p53-family-orchestrates-the-regulation-of-metabolism-physiological-regulation-and-implications-for-cancer-therapy
#9
REVIEW
Marco Napoli, Elsa R Flores
The p53 family of transcription factors is essential to counteract tumour formation and progression. Although previously this was exclusively associated with the ability of the p53 family to induce cell cycle arrest and apoptosis, an increasing number of reports have now indisputably demonstrated that the tumour suppressive functions of the p53 family members also rely on their ability to control and regulate cellular metabolism and maintain cellular oxidative homeostasis. Here, we review how each p53 family member, including p63 and p73, controls metabolic pathways in physiological conditions, and how these mechanisms could be exploited to provide anticancer therapeutic opportunities...
January 17, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/27600721/aggregation-tendencies-in-the-p53-family-are-modulated-by-backbone-hydrogen-bonds
#10
Elio A Cino, Iaci N Soares, Murilo M Pedrote, Guilherme A P de Oliveira, Jerson L Silva
The p53 family of proteins is comprised of p53, p63 and p73. Because the p53 DNA binding domain (DBD) is naturally unstable and possesses an amyloidogenic sequence, it is prone to form amyloid fibrils, causing loss of functions. To develop p53 therapies, it is necessary to understand the molecular basis of p53 instability and aggregation. Light scattering, thioflavin T (ThT) and high hydrostatic pressure (HHP) assays showed that p53 DBD aggregates faster and to a greater extent than p63 and p73 DBDs, and was more susceptible to denaturation...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27589690/the-dominant-negative-interplay-between-p53-p63-and-p73-a-family-affair
#11
Olivier Billant, Alice Léon, Solenn Le Guellec, Gaëlle Friocourt, Marc Blondel, Cécile Voisset
The tumor suppression activity of p53 is frequently impaired in cancers even when a wild-type copy of the gene is still present, suggesting that a dominant-negative effect is exerted by some of p53 mutants and isoforms. p63 and p73, which are related to p53, have also been reported to be subjected to a similar loss of function, suggesting that a dominant-negative interplay might happen between p53, p63 and p73. However, to which extent p53 hotspot mutants and isoforms of p53, p63 and p73 are able to interfere with the tumor suppressive activity of their siblings as well as the underlying mechanisms remain undeciphered...
October 25, 2016: Oncotarget
https://www.readbyqxmd.com/read/27549118/aggregation-and-prion-like-properties-of-misfolded-tumor-suppressors-is-cancer-a-prion-disease
#12
Danielly C F Costa, Guilherme A P de Oliveira, Elio A Cino, Iaci N Soares, Luciana P Rangel, Jerson L Silva
Prion diseases are disorders that share several characteristics that are typical of many neurodegenerative diseases. Recently, several studies have extended the prion concept to pathological aggregation in malignant tumors involving misfolded p53, a tumor-suppressor protein. The aggregation of p53 and its coaggregation with p53 family members, p63 and p73, have been shown. Certain p53 mutants exert a dominant-negative regulatory effect on wild-type (WT) p53. The basis for this dominant-negative effect is that amyloid-like mutant p53 converts WT p53 into an aggregated species, leading to a gain-of-function (GoF) phenotype and the loss of its tumor-suppressor function...
October 3, 2016: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/27447112/intrinsic-aggregation-propensity-of-the-p63-and-p73-ti-domains-correlates-with-p53r175h-interaction-and-suggests-further-significance-of-aggregation-events-in-the-p53-family
#13
Sebastian Kehrloesser, Christian Osterburg, Marcel Tuppi, Birgit Schäfer, Karen Heather Vousden, Volker Dötsch
The high percentage of p53 missense mutations found in cancer has been attributed to mutant acquired oncogenic gain of functions. Different aspects of these tumour-promoting functions are caused by repression of the transcriptional activity of p53 family members p63 and p73. A subset of frequently occurring p53 mutations results in thermodynamic destabilisation of the DNA-binding domain (DBD) rendering this domain highly unstable. These conformational mutants (such as p53R175H) have been suggested to directly bind to p63 and p73 via a co-aggregation mechanism mediated by their DBDs...
December 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27391430/%C3%AE-np63-mediates-cellular-survival-and-metastasis-in-canine-osteosarcoma
#14
Maren Cam, Heather L Gardner, Ryan D Roberts, Joelle M Fenger, Denis C Guttridge, Cheryl A London, Hakan Cam
p63 is a structural homolog within the 53 family encoding two isoforms, ΔNp63 and TAp63. The oncogenic activity of ΔNp63 has been demonstrated in multiple cancers, however the underlying mechanisms that contribute to tumorigenesis are poorly characterized. Osteosarcoma (OSA) is the most common primary bone tumor in dogs, exhibiting clinical behavior and molecular biology essentially identical to its human counterpart. The purpose of this study was to evaluate the potential contribution of ΔNp63 to the biology of canine OSA...
July 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27066457/oncogenic-intra-p53-family-member-interactions-in-human-cancers
#15
REVIEW
Maria Ferraiuolo, Silvia Di Agostino, Giovanni Blandino, Sabrina Strano
The p53 gene family members p53, p73, and p63 display several isoforms derived from the presence of internal promoters and alternative splicing events. They are structural homologs but hold peculiar functional properties. p53, p73, and p63 are tumor suppressor genes that promote differentiation, senescence, and apoptosis. p53, unlike p73 and p63, is frequently mutated in cancer often displaying oncogenic "gain of function" activities correlated with the induction of proliferation, invasion, chemoresistance, and genomic instability in cancer cells...
2016: Frontiers in Oncology
https://www.readbyqxmd.com/read/26925389/mutant-p53-and-ets2-a-tale-of-reciprocity
#16
REVIEW
Luis Alfonso Martinez
TP53 is one of the most frequently inactivated tumor suppressor genes in human cancer. However, unlike other tumor suppressor genes whose expression is lost, TP53 is usually inactivated as a result of a single nucleotide change within the coding region. Typically, these single nucleotide mutations result in a codon change that creates an amino acid substitution. Thus, unlike other tumor suppressor genes whose expression is lost due to genetic or epigenetic changes, the p53 gene primarily suffers missense mutations, and therefore, the cells retain and express a mutant form of the p53 protein (mtp53)...
2016: Frontiers in Oncology
https://www.readbyqxmd.com/read/26668111/dna-repair-and-aging-the-impact-of-the-p53-family
#17
REVIEW
Sara Nicolai, Antonello Rossi, Nicola Di Daniele, Gerry Melino, Margherita Annicchiarico-Petruzzelli, Giuseppe Raschellà
Cells are constantly exposed to endogenous and exogenous factors that threaten the integrity of their DNA. The maintenance of genome stability is of paramount importance in the prevention of both cancer and aging processes. To deal with DNA damage, cells put into operation a sophisticated and coordinated mechanism, collectively known as DNA damage response (DDR). The DDR orchestrates different cellular processes, such as DNA repair, senescence and apoptosis. Among the key factors of the DDR, the related proteins p53, p63 and p73, all belonging to the same family of transcription factors, play multiple relevant roles...
December 2015: Aging
https://www.readbyqxmd.com/read/26652033/novel-therapeutic-interventions-for-p53-altered-tumors-through-manipulation-of-its-family-members-p63-and-p73
#18
Avinashnarayan Venkatanarayan, Payal Raulji, William Norton, Elsa R Flores
TP53 is highly mutated in human cancers, thus targeting this tumor suppressor pathway is highly desirable and will impact many cancer patients. (1,2) Therapeutic strategies to reactivate the p53-pathway have been challenging, (3,4) and no effective treatment exists. (5) We utilized the p53-family members, p63 and p73, which are not frequently mutated in cancer, to treat p53-defective cancers. The N-terminal splice variants of p63 and p73 are denoted as the TA and ΔN isoforms. We recently demonstrated that deletion of either ΔNp63 or ΔNp73 in p53-deficient mouse tumors results in tumor regression mediated by metabolic programming...
2016: Cell Cycle
https://www.readbyqxmd.com/read/26518890/aspp-and-iaspp-implication-in-cancer-development-and-progression
#19
REVIEW
Y Li, A Ahmad, F H Sarkar
The well-known guardian of genome, p53 plays critical roles in the induction of apoptosis typically upon DNA damage whereas mutant p53 containing cells are unable to undergo apoptosis which leads to aggressive tumor growth and drug resistance. Moreover, another molecule regulating wild-ype p53 function is ASPP (apoptosis stimulating proteins of p53) family. ASPP family consists of ASPP1 and ASPP2, and functions as tumor suppressors whereas the inhibitor of ASPP (iASPP) functions as oncogene. By binding to apoptosis regulating proteins such as p53, p63, p73, Bcl-2, NF-κB p65, etc...
October 30, 2015: Cellular and Molecular Biology
https://www.readbyqxmd.com/read/26374530/p63-in-health-and-cancer
#20
REVIEW
Stefania Gonfloni, Valerio Caputo, Valentina Iannizzotto
TP63 is the most ancient member of the p53 gene family. The p53 family comprises three transcription factors (p53/p63/p73). They share a high degree of homology and similar domain structure. Yet, they can exist as truncated isoforms. Alternative promoters and splicing sites lead to the generation of several molecules. P53/p63/p73 are important to maintain cell homeostasis. P63 and p73 regulate many p53 target genes. This is due to their common structural features. Both proteins may compensate the loss of p53...
2015: International Journal of Developmental Biology
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