Relevant bibliographies by topics / ProteÃna p53

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Academic literature on the topic 'ProteÃna p53'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "ProteÃna p53"

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Estebanell, Eva, Aleix Cases, José López-Pedret, Ricardo Castillo, Antonio Ordinas, Ginés Escolar, and Maribel Diaz-Ricart. "Erythropoietin Improves Signaling through Tyrosine Phosphorylation in Platelets from Uremic Patients." Thrombosis and Haemostasis 82, no. 10 (1999): 1312–17. http://dx.doi.org/10.1055/s-0037-1614382.

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SummaryErythropoietin has shown to be effective in the correction of the hemostatic defect present in uremic patients. We have investigated the possible effect of recombinant human erythropoietin (rHuEPO) on the signaling processes occurring in platelets. Platelet suspensions were obtained from hemodialyzed patients before and after at least one month of initiating treatment with rHuEPO. Aliquots of non-activated or thrombin-activated platelets were treated to obtain platelet lysates or processed to extract platelet cytoskeleton. Samples were resolved by 8% SDS-polyacrylamide gel electrophoresis followed by Western blotting. After thrombin activation, proteins p120, p85, p78, p75, pp62, pp60, p59, p58, p56, p54 and p52 associated with the Triton-insoluble cytoskeletal fraction appeared phosphorylated in control profiles. In profiles from platelets obtained from uremic patients before treatment with rHuEPO, only proteins p58 and p56 appeared clearly and p54 was slightly phosphorylated. However, in platelets from the same patients under rHuEPO treatment, thrombin-induced phosphorylation improved to levels even above those observed in control profiles. Specially, the band at 54KDa appeared consistently more phosphorylated in all the patients under rHuEPO treatment. Although it is accepted that part of the hemostatic effect of erythropoietin is mediated by an increase in hematocrit, our study suggests that it enhances platelet signaling in uremic platelets which may explain the improvement of platelet response to activating stimulus before clinically noticeable elevation of hematocrit. Abbrevations: rHuEPO = recombinant human erythropoietin; SDS-PAGE = sodium dodecyl sulphate-polyacrylamide gel electrophoresis; CPD = citrate/phosphate/dextrose; PRP = platelet-rich plasma; HBSS = Hanks’ balanced salt solution; EGTA = ethylene glycol bis (β-aminoethylether)-N,N,N’,N’-tetraacetic acid; EDTA = ethylenediaminetetraacetic acid, PMSF = phenylmethylsulphonyl fluoride, ECL = enhanced chemiluminiscence
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Ashcroft, Margaret, Michael H. G. Kubbutat, and Karen H. Vousden. "Regulation of p53 Function and Stability by Phosphorylation." Molecular and Cellular Biology 19, no. 3 (March 1, 1999): 1751–58. http://dx.doi.org/10.1128/mcb.19.3.1751.

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ABSTRACT The p53 tumor suppressor protein can be phosphorylated at several sites within the N- and C-terminal domains, and several protein kinases have been shown to phosphorylate p53 in vitro. In this study, we examined the activity of p53 proteins with combined mutations at all of the reported N-terminal phosphorylation sites (p53N-term), all of the C-terminal phosphorylation sites (p53C-term), or all of the phosphorylation sites together (p53N/C-term). Each of these mutant proteins retained transcriptional transactivation functions, indicating that phosphorylation is not essential for this activity of p53, although a subtle contribution of the C-terminal phosphorylation sites to the activation of expression of the endogenous p21Waf1/Cip1-encoding gene was detected. Mutation of the phosphorylation sites to alanine did not affect the sensitivity of p53 to binding to or degradation by Mdm2, although alteration of residues 15 and 37 to aspartic acid, which could mimic phosphorylation, resulted in a slight resistance to Mdm2-mediated degradation, consistent with recent reports that phosphorylation at these sites inhibits the p53-Mdm2 interaction. However, expression of the phosphorylation site mutant proteins in both wild-type p53-expressing and p53-null lines showed that all of the mutant proteins retained the ability to be stabilized following DNA damage. This indicates that phosphorylation is not essential for DNA damage-induced stabilization of p53, although phosphorylation could clearly contribute to p53 stabilization under some conditions.
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Wienzek, Sandra, Judith Roth, and Matthias Dobbelstein. "E1B 55-Kilodalton Oncoproteins of Adenovirus Types 5 and 12 Inactivate and Relocalize p53, but Not p51 or p73, and Cooperate with E4orf6 Proteins To Destabilize p53." Journal of Virology 74, no. 1 (January 1, 2000): 193–202. http://dx.doi.org/10.1128/jvi.74.1.193-202.2000.

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ABSTRACT The p53 tumor suppressor protein represents a target for viral and cellular oncoproteins, including adenovirus gene products. Recently, it was discovered that several proteins with structural and functional homologies to p53 exist in human cells. Two of them were termed p51 and p73. We have shown previously that the E1B 55-kDa protein (E1B-55 kDa) of adenovirus type 5 (Ad5) binds and inactivates p53 but not p73. Further, p53 is rapidly degraded in the presence of E1B-55 kDa and the E4orf6 protein of this virus. Here, it is demonstrated that p51 does not detectably associate with E1B-55 kDa. While p53 is relocalized to the cytoplasm by E1B-55 kDa, p51's location is unaffected. Finally, p51 retains its full transcriptional activity in the presence of E1B-55 kDa. Apparently, p51 does not represent a target of Ad5 E1B-55 kDa, suggesting that the functions of p51 are distinct from p53-like tumor suppression. E1B-55 kDa from highly oncogenic adenovirus type 12 (Ad12) was previously shown to surpass the oncogenic activity of Ad5 E1B-55 kDa in various assay systems, raising the possibility that Ad12 E1B-55 kDa might target a broader range of p53-like proteins. However, we show here that Ad12 E1B-55 kDa also inhibits p53's transcriptional activity without measurably affecting p73 or p51. Moderate inhibition of p51's transcriptional activity was observed in the presence of the E4orf6 proteins from Ad5 and Ad12. p53 and Ad12-E1B-55 kDa colocalize in the nucleus and also in cytoplasmic clusters when transiently coexpressed. Finally, E1B-55 kDa and E4orf6 of Ad12 mediate rapid degradation of p53 with an efficiency comparable to that of the Ad5 proteins in human and rodent cells. Our results suggest that E1B-55 kDa of either virus type has similar effects on p53 but does not affect p73 and p51.
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Legagneux, V., P. Bouvet, F. Omilli, S. Chevalier, and H. B. Osborne. "Identification of RNA-binding proteins specific to Xenopus Eg maternal mRNAs: association with the portion of Eg2 mRNA that promotes deadenylation in embryos." Development 116, no. 4 (December 1, 1992): 1193–202. http://dx.doi.org/10.1242/dev.116.4.1193.

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Maternal Xenopus Eg mRNAs have been previously identified as transcripts that are specifically deadenylated after fertilization and degraded after the mid blastula transition. Destabilizing cis sequences were previously localised in the 3′ untranslated region of Eg2 mRNA. In order to characterize possible trans-acting factors which are involved in the post-transcriptional regulation of Eg mRNAs, gel-shift and u.v. cross-linking experiments were performed, which allowed the identification of a p53-p55 RNA-binding protein doublet specific for the 3′ untranslated regions of Eg mRNAs. These p53-p55 proteins do not bind to the 3′ untranslated regions of either ornithine decarboxylase or phosphatase 2Ac mRNAs, which remain polyadenylated in embryos. These novel RNA-binding proteins are distinct from the cytoplasmic polyadenylation element-binding protein that controls the polyadenylation of maternal mRNAs in maturing Xenopus oocytes, and from previously identified thermoresistant RNA-binding proteins present in oocyte mRNP storage particles. The p53-p55 bind a portion of the Eg2 mRNA 3′ untranslated region, distinct from the previously identified destabilizing region, that is able to confer the postfertilization deadenylation of CAT-coding chimeric mRNAs. This suggests that the p53-p55 RNA-binding proteins are good candidates for trans-acting factors involved in the deadenylation of Eg mRNAs in Xenopus embryos.
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Porubiaková, Otília, Natália Bohálová, Alberto Inga, Natália Vadovičová, Jan Coufal, Miroslav Fojta, and Václav Brázda. "The Influence of Quadruplex Structure in Proximity to P53 Target Sequences on the Transactivation Potential of P53 Alpha Isoforms." International Journal of Molecular Sciences 21, no. 1 (December 24, 2019): 127. http://dx.doi.org/10.3390/ijms21010127.

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p53 is one of the most studied tumor suppressor proteins that plays an important role in basic biological processes including cell cycle, DNA damage response, apoptosis, and senescence. The human TP53 gene contains alternative promoters that produce N-terminally truncated proteins and can produce several isoforms due to alternative splicing. p53 function is realized by binding to a specific DNA response element (RE), resulting in the transactivation of target genes. Here, we evaluated the influence of quadruplex DNA structure on the transactivation potential of full-length and N-terminal truncated p53α isoforms in a panel of S. cerevisiae luciferase reporter strains. Our results show that a G-quadruplex prone sequence is not sufficient for transcription activation by p53α isoforms, but the presence of this feature in proximity to a p53 RE leads to a significant reduction of transcriptional activity and changes the dynamics between co-expressed p53α isoforms.
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Chen, Jing, Dadong Zhang, Xiaodi Qin, Kouros Owzar, Jennifer J. McCann, and Michael B. Kastan. "DNA-Damage-Induced Alternative Splicing of p53." Cancers 13, no. 2 (January 12, 2021): 251. http://dx.doi.org/10.3390/cancers13020251.

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Cellular responses to DNA damage and other stresses are important determinants of mutagenesis and impact the development of a wide range of human diseases. TP53 is highly mutated in human cancers and plays an essential role in stress responses and cell fate determination. A central dogma of p53 induction after DNA damage has been that the induction results from a transient increase in the half-life of the p53 protein. Our laboratory recently demonstrated that this long-standing paradigm is an incomplete picture of p53 regulation by uncovering a critical role for protein translational regulation in p53 induction after DNA damage. These investigations led to the discovery of a DNA-damage-induced alternative splicing (AS) pathway that affects p53 and other gene products. The damage-induced AS of p53 pre-mRNA generates the beta isoform of p53 (p53β) RNA and protein, which is specifically required for the induction of cellular senescence markers after ionizing irradiation (IR). In an attempt to elucidate the mechanisms behind the differential regulation and apparent functional divergence between full-length (FL) p53 and the p53β isoform (apoptosis versus senescence, respectively), we identified the differential transcriptome and protein interactome between these two proteins that may result from the unique 10-amino-acid tail in p53β protein.
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Roth, Judith, and Matthias Dobbelstein. "Failure of viral oncoproteins to target the p53-homologue p51A." Journal of General Virology 80, no. 12 (December 1, 1999): 3251–55. http://dx.doi.org/10.1099/0022-1317-80-12-3251.

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The p51/p63/KET proteins were identified based on their strong homology to the tumour suppressor p53 and a related set of proteins termed p73. All these protein species were shown to activate transcription from at least some p53-responsive promoters. To evaluate a possible role of the transcriptionally active splicing variant p51A/p63γ in tumour suppression, we determined whether viral oncoproteins that inactivate p53 might also target p51A. Neither the large T-antigen of simian vacuolating virus 40 (SV40) nor the E6 protein from human papillomavirus type 18 were found to inhibit p51A-mediated transcription, whereas they strongly suppress the activity of p53. Further, SV40 T-antigen directly interacts with p53 but not detectably with p51A. Finally, a cytoplasmic mutant (K128A) of SV40 T-antigen relocalizes p53 from the nucleus to the cytoplasm, but p51A remains in the nucleus when coexpressed with cytoplasmic T-antigen. These results strongly suggest that the inhibitory effect of these viral oncoproteins is specific for p53 and does not measurably affect p51A. Thus, unlike p53, p51A does not appear to be a necessary target in virus-induced cell transformation and may not exert a role comparable to p53 in tumour suppression.
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Martinou, I., P. A. Fernandez, M. Missotten, E. White, B. Allet, R. Sadoul, and J. C. Martinou. "Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation." Journal of Cell Biology 128, no. 1 (January 1, 1995): 201–8. http://dx.doi.org/10.1083/jcb.128.1.201.

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To study molecular mechanisms underlying neuronal cell death, we have used sympathetic neurons from superior cervical ganglia which undergo programmed cell death when deprived of nerve growth factor. These neurons have been microinjected with expression vectors containing cDNAs encoding selected proteins to test their regulatory influence over cell death. Using this procedure, we have shown previously that sympathetic neurons can be protected from NGF deprivation by the protooncogene Bcl-2. We now report that the E1B19K protein from adenovirus and the p35 protein from baculovirus also rescue neurons. Other adenoviral proteins, E1A and E1B55K, have no effect on neuronal survival. E1B55K, known to block apoptosis mediated by p53 in proliferative cells, failed to rescue sympathetic neurons suggesting that p53 is not involved in neuronal death induced by NGF deprivation. E1B19K and p35 were also coinjected with Bcl-Xs which blocks Bcl-2 function in lymphoid cells. Although Bcl-Xs blocked the ability of Bcl-2 to rescue neurons, it had no effect on survival that was dependent upon expression of E1B19K or p35.
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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 (March 1, 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 for aberrant chaperone interactions in mediating the altered function of mutant p53 and its intracellular accumulation, we examined the chaperone proteins which physically associate with a temperature-sensitive murine p53 mutant. In lysate prepared from A1-5 cells grown under mutant temperature conditions, hsp70 coprecipitated with p53Val135 as previously reported by others, but in addition, other well-recognized elements of the cellular chaperone machinery, including hsp90, cyclophilin 40, and p23, were detected. Under temperature conditions favoring wild-type p53 conformation, the coprecipitation of chaperone proteins with p53 was lost in conjunction with the restoration of its transcriptional activating activity. Chaperone interactions similar to those demonstrated in A1-5 cells under mutant conditions were also detected in human breast cancer cells expressing two different hot-spot mutations. To examine the effect of directly disrupting chaperone interactions with mutant p53, we made use of geldanamycin (GA), a selective hsp90-binding agent which has been shown to alter the chaperone associations regulating the function of unliganded steroid receptors. GA treatment of cells altered heteroprotein complex formation with several different mutant p53 species. It increased p53 turnover and resulted in nuclear translocation of the protein in A1-5 cells. GA did not, however, appear to restore wild-type transcriptional activating activity to mutant p53 proteins in either A1-5 cells or human breast cancer cell lines.
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Dao, Thi Nguyet Minh, Sung-Hwan Kang, Aurélie Bak, and Svetlana Y. Folimonova. "A Non-Conserved p33 Protein of Citrus Tristeza Virus Interacts with Multiple Viral Partners." Molecular Plant-Microbe Interactions® 33, no. 6 (June 2020): 859–70. http://dx.doi.org/10.1094/mpmi-11-19-0328-fi.

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The RNA genome of citrus tristeza virus (CTV), one of the most damaging viral pathogens of citrus, contains 12 open reading frames resulting in production of at least 19 proteins. Previous studies on the intraviral interactome of CTV revealed self-interaction of the viral RNA-dependent RNA polymerase, the major coat protein (CP), p20, p23, and p33 proteins, while heterologous interactions between the CTV proteins have not been characterized. In this work, we examined interactions between the p33 protein, a nonconserved protein of CTV, which performs multiple functions in the virus infection cycle and is needed for virus ability to infect the extended host range, with other CTV proteins shown to mediate virus interactions with its plant hosts. Using yeast two-hybrid, bimolecular fluorescence complementation, and coimmunoprecipitation assays, we demonstrated that p33 interacts with three viral proteins, i.e., CP, p20, and p23, in vivo and in planta. Coexpression of p33, which is an integral membrane protein, resulted in a shift in the localization of the p20 and p23 proteins toward the subcellular crude-membrane fraction. Upon CTV infection, the four proteins colocalized in the CTV replication factories. In addition, three of them, CP, p20, and p23, were found in the p33-formed membranous structures. Using bioinformatic analyses and mutagenesis, we found that the N-terminus of p33 is involved in the interactions with all three protein partners. A potential role of these interactions in virus ability to infect the extended host range is discussed.
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Dissertations / Theses on the topic "ProteÃna p53"

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AndrÃ, Angela Rosa. "AssociaÃÃo da presenÃa de Helicobacter pylori e dos genÃtipos caga e vaca com as alteraÃÃes moleculares dos supressores tumorais P53 e P27 nos adenocarcinomas gÃstricos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1819.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
O carcinoma gÃstrico à a segunda causa de morte por cÃncer no mundo. No Cearà à o segundo mais freqÃente entre os homens e o terceiro entre as mulheres. Dos cÃnceres gÃstricos os adenocarcinomas representam em torno de 95%. A doenÃa tem sido associada a fatores genÃticos e ambientais sendo demonstrada Ãntima relaÃÃo com a infecÃÃo por Helicobacter pylori, principalmente associada à presenÃa do gene cagA e genÃtipos vacAs1m1. Entretanto, apesar dos mecanismos pelos quais a bactÃria promove a carcinogÃnese gÃstrica ainda nÃo estarem esclarecidos, uma das hipÃteses seria atravÃs da inativaÃÃo de supressores tumorais. O objetivo do presente trabalho foi verificar, em adenocarcinomas gÃstricos, se a presenÃa de H. pylori, e de seus genes cagA e vacA, està relacionada com a mutaÃÃo e/ou alteraÃÃo na expressÃo protÃica dos supressores tumorais p53 e p27. Neste estudo, 74 amostras de pacientes foram analisadas quanto à presenÃa de H. pylori, cagA+ e os genÃtipos de vacA, pela reaÃÃo em cadeia da polimerase (PCR). A anÃlise mutacional do gene p53 foi realizada por PCR-SSCP e a detecÃÃo da mutaÃÃo/superexpressÃo do p53 e expressÃo da proteÃna p27 pelo mÃtodo imunohistoquÃmico. A bactÃria foi detectada em 95% das amostras, das quais 63% eram cagA(+). Dentre os alelos de vacA, observou-se predomÃnio de s1 (74%) e m1 (82%), associados em 69% dos casos. Na anÃlise mutacional do p53 verificou-se que 72% dos casos exibiram alteraÃÃo no padrÃo de mobilidade eletroforÃtica, sendo esta associada significativamente à presenÃa do gene cagA. Por outro lado, apenas 29% dos casos apresentaram detecÃÃo pelo mÃtodo imunohistoquÃmico, nÃo sendo encontrada associaÃÃo com a H. pylori. A proteÃna p27 demonstrou acentuada reduÃÃo em sua expressÃo (detectada em apenas 19% dos casos), nÃo demonstrando atividade compensatÃria em relaÃÃo à proteÃna p53 mutada e sem associaÃÃo estatÃstica dos casos negativos com a presenÃa da H. pylori. Finalmente, os resultados sugerem que estes supressores simultaneamente inativados podem ser o ponto chave da desregulaÃÃo do ciclo celular que, associados a outros fatores, favoreÃam o desenvolvimento e progressÃo dos adenocarcinomas gÃstricos. Hà indÃcios de que a presenÃa bacteriana, e dos seus genes cagA(+) e vacA/s1m1, possam influenciar, de forma nÃo esclarecida, as alteraÃÃes moleculares ocorridas nos supressores tumorais p53 e p27.
Gastric carcinoma is the second cause of death by cancer in the world. On State of Ceara-Brazil is the second most frequent type of cancer in men and third in women. Adenocarcinomas account for approximately 95% of all malignant gastric neoplasms. It has been associated to genetic and environmental factors and a intimate relationship between the infection by the bacteria Helicobacter pylori and the gastric carcinoma have been related. The presence of the cagA gene and specific genotypes (s1m1) of the gene vacA have been detected in more pathogenic strains. Although the precise molecular mechanisms by which H. pylori could promote the process of gastric carcinogenesis are under investigation, one hypothesized mechanism involves the tumor supressor genes inactivation. The aim of the present study was to verify if the presence of Helicobacter pylori, cagA and vacA genes is related to mutations in the tumor supressor gene p53 and altered expression of p53 and p27 proteins in gastric adenocarcinomas. Seventy-four (74) samples were analyzed to detect the presence of H. pylori, cagA and genotypes of vacA by Polymerization Chain Reaction (PCR). The mutational analysis of p53 gene was performed by PCR-SSCP (Polymerization Chain Reaction for analysis of the Single-strand Conformation Polymorphism). Analysis of mutation or overexpression of p53 protein and p27 expression was detected by the immunohistochemical method. The bacteria was detected in 95% of the samples, 63% was cagA(+). Among the vacA allele it was observed prevalence of s1 (74%) and m1 (82%), associated in 69% of the cases. Mutation analysis of p53 demonstrated 72% of the cases with altered electrophoretic mobility; The alterations were significatively more frequent in the presence of the cagA gene. Immunohistochemical analysis detected only 29% of cases with the expression of p53 protein. The protein p27 showed accentuated reduction in its expression (detected in only 19% of the cases), it has not demonstrated compensatory activity in relation to the p53 altered protein, neither association to H. pylori presence. Finally, these data suggest that simultaneous inactivation of these tumor suppressors genes may be the key point of deregulation of the cellular cycle that, associated to the other factors, favor the development and progression of the gastric cancer. There is some evidence that the bacterial presence, cagA and vacA/s1m1 genes, may influence, in a not understood way, the alterations observed in the tumor suppressors p53 and p27.
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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 proliferation and survival, yet exactly why mutant p53s acquire oncogenic activity is still poorly understood. Mutant p53 has also been found to complex with wildtype p53, thus acting in a dominant negative way. However, this inhibition is incomplete since many cancers with mutant p53 alleles also have a loss of the second wild-type p53 allele and thus only express the mutant p53 (Baker et al., 1989). An N-terminal truncated p53 isoform, p47, arising from alternative splicing of the p53 gene (Ghosh et al., 2004) or by alternative initiation sites for translation (Yin et al. , 2002), has been described. Alternative splicing was found to be universal in all human multi-exon genes (Wang et al., 2008) and therefore determining the role of the p47 isoform with respect to the p53 gene is essential. Evidence in this study suggests that mutant p53 (p53RI75H) has a similar structure and function as p47, including the ability to complex with and impair both p53 and p73. Therefore, in addition to expressing a tumour suppressor protein, the p53 gene can also express an onco-protein (p47). This study therefore argues that tumours select for mutant p53 because it has gained the ability to function like p47, a wild-type p53 isoform.
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Xie, Tian. "Scintillation proximity assay (SPA) measuring p53 DNA binding and total p53 level in human thyroid cancer cell line ARO." Diss., Online access via UMI:, 2007.

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

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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. Hlavním cílem experimentální části byla produkce čtyř mutantních forem proteinů p53 a wild-type p53 proteinu a studium jejich vazebných vlastnosti s různými lokálními sekundárními strukturami DNA. Pomoci Gateway klonovacího systému byly připraveny čtyři expresní vektory, které byly použity pro produkci proteinů v bakteriálním expresním systému. Celkem byly úspěšně připraveny čtyři mutantní formy a wild-type p53 protein. Jejich vazebné vlastnosti byly studovány gelovou retardační analýzu. Výsledky naznačují různé DNA-vazebné vlastnosti wild-type p53 a studovaných mutantních forem tohoto proteinu. Všechny mutantní proteiny ztratily schopnost sekvenčně specificky vázat DNA, zatímco nespecifická interakce s DNA byla pozorována u tří ze čtyř mutantních forem. Jeden ze studovaných mutantních proteinů se vázal jenom na superhelikální formu DNA.
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Cossi, Lucas Bahdour. "Detecção das proteínas p53, p63 e puma no carcinoma de células escamosas corneal de cães / Lucas Bahdour Cossi. -." Araçatuba, 2013. http://hdl.handle.net/11449/92182.

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Orientador: Alexandre Lima de Andrade
Banca: Silmara Sanae Sakamoto de Lima
Banca: Flávia Rezende Eugênio
Resumo: As neoplasias oculares representam uma crescente preocupação na oftalmologia veterinária. O carcinoma de células escamosas (CCE) corneal é raro em cães, pouco estudado e as investigações sobre os mecanismos da carcinogênese são escassos. O presente trabalho teve por objetivo avaliar a imunoexpressão das proteínas p53, p63 e PUMA e suas possíveis contribuições quanto ao prognóstico e terapêutica no CCE corneal espontâneo de cães. Foram identificados seis casos, cinco diagnosticados como CCE e um como ceratite actínica. Na imunoistoquímica avaliou-se o número de células marcadas por campo no microscópio adotando-se dois critérios de classificação, quanto à intensidade e quanto à frequência de marcação. Também foi avaliada a graduação histológica dos tumores quanto ao grau de malignidade nos casos de carcinoma de células escamosas de córnea, utilizando o índice mitótico como principal referência. Todas as amostras apresentaram imunomarcação para as proteínas estudadas, porém com intensidade e frequência variadas. Não foi observada relação entre maior índice mitótico e, portanto, maior malignidade, com uma maior expressão de qualquer uma das proteínas analisadas. Conclui-se que a imunoexpressão das proteínas p53, p63 e PUMA estão presentes nos CCE corneal de cães podendo contribuir para sua carcinogênese, mas não fornece indicadores de prognóstico nesta neoplasia
Abstract: Ocular tumors play an increasing concern in veterinary ophthalmology. Corneal squamous cell carcinoma (SCC) is unfrequent in dogs, and by this way it has little studies, and the investigations of carcinogenesis mechanisms are rare. The aim of this work was to identify the p53, p63 and PUMA proteins expression in the spontaneous dog corneal SCC. For this work, were used five cases of corneal SCC and one case of actinic keratitis and their possible contributions to prognosis and therapy. The immunohistochemical analysis could evaluated the number of stained cells by field in optic microscopy using two classifications methods: intensity and immunofrequency. Also, we could evaluated histological grade of tumor related to malignancy in corneal SCC cells by using the mitotic index as a pattern. All samples showed immunolabelling to those proteins studied, although with diversity in intensity and frequency. The authors couldn't observe relationship between the biggest mitotic index, and, by this way, most malignancy, with the expressions of all analysed proteins. These results could support the conclusions that p53, p63 and PUMA proteins immunoexpression are present in canine corneal SCC and could give help to their carcinogenesis, but they don't give a prognostic indicator of these tumors
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Cossi, Lucas Bahdour [UNESP]. "Detecção das proteínas p53, p63 e puma no carcinoma de células escamosas corneal de cães: Lucas Bahdour Cossi. -." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/92182.

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Ocular tumors play an increasing concern in veterinary ophthalmology. Corneal squamous cell carcinoma (SCC) is unfrequent in dogs, and by this way it has little studies, and the investigations of carcinogenesis mechanisms are rare. The aim of this work was to identify the p53, p63 and PUMA proteins expression in the spontaneous dog corneal SCC. For this work, were used five cases of corneal SCC and one case of actinic keratitis and their possible contributions to prognosis and therapy. The immunohistochemical analysis could evaluated the number of stained cells by field in optic microscopy using two classifications methods: intensity and immunofrequency. Also, we could evaluated histological grade of tumor related to malignancy in corneal SCC cells by using the mitotic index as a pattern. All samples showed immunolabelling to those proteins studied, although with diversity in intensity and frequency. The authors couldn´t observe relationship between the biggest mitotic index, and, by this way, most malignancy, with the expressions of all analysed proteins. These results could support the conclusions that p53, p63 and PUMA proteins immunoexpression are present in canine corneal SCC and could give help to their carcinogenesis, but they don´t give a prognostic indicator of these tumors
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Chandrachud, Uma. "Differential interaction of wild type and mutant p53 to promoter sequences and analysis of interacting proteins." Diss., Online access via UMI:, 2009.

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Hellborg, Fredrik. "Identification, cloning and characterization of the p53 induced gene human wig-1 /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-190-3/.

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Lascani, Monsalve Jorge Andrés. "Producción recombinante de péptidos con potencial terapéutico en Escherichia coli." Tesis, Universidad de Chile, 2014. http://repositorio.uchile.cl/handle/2250/131760.

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Magíster en Ciencias de la Ingeniería, Mención Química
Ingeniero Civil en Biotecnología
Durante las últimas décadas, una rama de la investigación biotecnológica se ha enfocado en desarrollar y optimizar procesos de producción de proteínas recombinantes orientadas a aplicaciones terapéuticas. En particular, los péptidos terapéuticos ofrecen actualmente un nuevo potencial comercial para la industria farmacéutica y biotecnológica al generar estrategias efectivas en el tratamiento de diversas patologías como cáncer y alteraciones metabólicas entre otras. Estudios previos han demostrado la capacidad supresora de tumores de péptidos con blanco intracelular como p53p-Ant y PNC-27. Estos corresponden a regiones derivadas de la proteína p53, factor de regulación transcripcional que inhibe la progresión del ciclo celular e induce reparación celular o apoptosis, en caso de estrés genotóxico. Ambos péptidos contienen en su secuencia, un péptido de penetración celular, el cual les entrega la capacidad de atravesar la membrana plasmática. Así, bajo distintos mecanismos, con p53p-Ant y PNC-27 se ha reportado apoptosis o bien necrosis de manera selectiva en ciertos tipos de células tumorales. El presente trabajo tuvo por objetivo expresar en E. coli los péptidos p53p-Ant y PNC-27, y purificarlos mediante el sistema IMPACT. Éste es un mecanismo de expresión y purificación mediado por inteínas que permite purificar a través de una columna de afinidad, proteínas recombinantes con su secuencia nativa sin el uso de proteasas y minimizando pasos cromatográficos. Se logró producir ambos péptidos en forma soluble. La expresión soluble del péptido PNC-27 se consiguió a partir de los dos vectores de expresión proporcionados por el sistema IMPACT (pTXB1 y pTYB11), esta expresión resultó ser fuertemente dependiente de las condiciones de cultivo ya que se requiere de una inducción a baja temperatura (12 °C). Por su parte, la expresión soluble de p53p-Ant depende tanto del sistema de expresión como de las condiciones de cultivo. El diseño de las construcciones genéticas, en particular las que incluyen el vector de expresión pTYB11, permitió una efectiva purificación de los péptidos utilizando un único paso cromatográfico. Más aún, los niveles de rendimiento (0,4 1,2 mg L-1) superan los reportados para péptidos con el mismo sistema y los niveles de pureza obtenidos permitirían desarrollar investigación avanzada con ensayos biológicos in vivo o in vitro.
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Books on the topic "ProteÃna p53"

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The p53 tumor suppressor pathway and cancer. New York: Springer, 2005.

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p53. Austin, Texas, USA: Landes Bioscience, 2011.

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A, Maxwell Steven, and Roth Jack A, eds. p53 suppressor gene. New York: Springer-Verlag, 1995.

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Jianmin, Chen. p53 protein expression in murine embryonic stem cells. Ottawa: National Library of Canada, 1993.

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service), SpringerLink (Online, ed. Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53. Tokyo: Springer Japan, 2012.

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Levesque, Michael Anthony. Immunoreactive P53 protein as a prognostic indicator in ovarian carcinoma. Ottawa: National Library of Canada, 1996.

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Kamada, Rui. Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54135-6.

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Jenner, Keely. The detection and typing of human papillomavirus and p53 protein expression in malignant and non-maliognant oesophageal tissue. [s.l.]: typescript, 1998.

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Shartava, Tsisana. DNA research, genetics, and cell biology. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Zambetti, Gerard P. The p53 Tumor Suppressor Pathway and Cancer. Springer, 2014.

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Book chapters on the topic "ProteÃna p53"

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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, 223–32. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-2922-6_10.

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Maclaine, Nicola J., and Theodore Hupp. "The Regulation of p53 Protein Function by Phosphorylation." In p53, 53–64. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-8231-5_4.

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Ghaleb, Amr, and Natalia Marchenko. "p53-Hsp90 Axis in Human Cancer." In Heat Shock Proteins, 145–58. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-23158-3_7.

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Gu, Wei, Jianyuan Luo, Chris L. Brooks, Anatoly Y. Nikolaev, and Muyang Li. "Dynamics of the p53 Acetylation Pathway." In Reversible Protein Acetylation, 197–207. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470862637.ch14.

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Khoury, Kareem, Tad A. Holak, and Alexander Dömling. "p53/MDM2 Antagonists: Towards Nongenotoxic Anticancer Treatments." In Protein-Protein Interactions in Drug Discovery, 129–63. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527648207.ch7.

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Appella, Ettore, Kazuyasu Sakaguchi, Hiroshi Sakamoto, Marc S. Lewis, James G. Omichinski, Angela M. Gronenborn, G. Marius Clore, and Carl W. Anderson. "The P53 Tumor Suppressor Protein." In Methods in Protein Structure Analysis, 407–18. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1031-8_36.

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Mukhopadhyay, Tapas, Steven A. Maxwell, and Jack A. Roth. "Biophysical and Biochemical Properties of the p53 Protein." In p53 Suppressor Gene, 55–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22275-1_4.

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Marcel, Virginie, Marie P. Khoury, Kenneth Fernandes, Alexandra Diot, David P. Lane, and Jean-Christophe Bourdon. "Detecting p53 Isoforms at Protein Level." In Methods in Molecular Biology, 15–29. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-236-0_2.

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Finan, Peter M., and Stephen G. Ward. "PI3-Kinase Inhibition." In Protein Tyrosine Kinases, 53–69. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59259-962-1:053.

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Harrington, R. E., V. B. Zhurkin, S. R. Durell, R. L. Jernigan, A. K. Nagaich, and E. Appella. "A Structural Model for the P53 Complex with DNA Response Elements: Implications for P53 Function and Future Research Directions." In Proteome and Protein Analysis, 257–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59631-5_19.

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Conference papers on the topic "ProteÃna p53"

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Shin, Yong-Jun, Steven M. Lipkin, Brandon Hencey, and Xiling Shen. "Disturbance Rejection Helps Modulate the p53 Oscillation." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6046.

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Designing a system that adequately processes the input and that rejects the effects of disturbance is a central theme in feedback control theory. In this paper, we use the concept of “disturbance rejection” to analyze the oscillatory behavior of p53, a well-known tumor suppressor protein. Our analysis reveals that the p53 oscillation is not completely dictated by the p53-MDM2 negative feedback loop—it is also modulated by periodic DNA repair-related fluctuations. According to our disturbance rejection model, the feedback loop normally filters the effects of noise and fluctuations on p53, but upon DNA damage, it stops performing the filtering function so that DNA repair-related fluctuations can modulate the p53 oscillation. Our analysis suggests that the overexpression of MDM2, observed in many types of cancer, can make the feedback mechanism less responsive to the modulating signals after DNA damage occurs.
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Zhao, Yuhan, Cen Zhang, Xuetian Yue, Xiaoyan Li, Juan Liu, Haiyang Yu, Qifeng Yang, Zhaohui Feng, and Wenwei Hu. "Abstract 1221: Pontin, a new mutant p53 binding protein, promotes gain-of-function of mutant p53." In 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.

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Salazar, A. M. "Expression of P53 protein after exposure to ionizing radiation." In MEDICAL PHYSICS: Fifth Mexican Symposium. AIP, 2001. http://dx.doi.org/10.1063/1.1420483.

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Akande, Oluwatoyin E., Priyadarshan K. Damle, Nicholas E. Sherman, and Steven R. Grossman. "Abstract 2571: DBC1, a novel CBP-interacting protein, promotes p53 stability by regulating CBP-dependent p53 polyubiquitination." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2571.

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Lee, Min-Gyu, Jae-Cheol Lee, Ki-Hong Nam, Jihee Yoo, Jeehun Park, and Jeung-Whan Han. "Abstract C192: Protein L-isoaspartyl methyltransferase negatively regulates p53 activity." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c192.

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Ben Slama, S., D. Bacha, A. Ben Amor, A. Halouani, and A. Lahmar. "54 Prognostic value of p53 protein expression in breast cancer." In IGCS 2020 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-igcs.53.

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Karki, Anju, Khashayar Vakili, and Antonio R. Perez-Atayde. "Abstract B37: Assessing DNA damage response pathway proteins ATM and p53 in fibrolamellar hepatocellular carcinoma with PRKACA-DNAJB1 fusion protein." In Abstracts: AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; December 3-6, 2017; Atlanta, Georgia. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.pedca17-b37.

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Abdullah, Saad, Mauro Serpelloni, Sarah Tonello, Emilio Sardini, Giulia Abate, and Daniela Uberti. "Spectrophotometer measurements to characterize conformational state of the proteins: p53 analysis." In 2018 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2018. http://dx.doi.org/10.1109/memea.2018.8438807.

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Karniguian, A., F. Rendu, F. Grelac, and Y. J. Legrand. "COLLAGEN-DERIVED OCTAPEPTIDE (OP) AND INITIAL EVENTS OF PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644478.

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A collagen-derived OP was shown to specifically inhibit collagen induced platelet aggregation, fibrinogen binding and prothrombinase activity, suggesting that it affects on the iniating mechanism. In view of this, early biochemical steps were investigating in platelet response to collagen and OP. In the absence of external calcium, a transient decrease in 32Pphosphatidy14,5,bisphosphate (PIP2) occuring in parallel with the shape change, but partially preceding it, was followed by a rapid resynthesis up to 25%. A slightly delayed hydrolysis of PIP also occured within seconds of platelet aggregation. Phosphatidate (PA) was produced only at a small extent , even with high doses of collagen. The phosphorylation of myosin light chain (P20) was minimal, whereas, the phosphorylation of the 43K protein (P43) occured and increased inparallel with the onset of secretion and aggregation, and was collagen dosedependent. Pretreatement by OP reduced the platelet responsiveness and parallely the P43 phosphorylation up to 80%.At concentrations allowing shape change but not aggregation, the breakdown of PIP2 persisted, and only the resynthesis was affected; high doses of OP which prevented any shape change, no PIP2 cleavage was observed.PA formation and P20 phosphorylation were slightly inhibited by 30-50% only at these high doses which completely abolished the PIP2 breakdown.Thus OP could inhibit P43 phosphorylation and platelet aggregation at a concentration which did not affect the ' PIP2-specific phospholipase C. This suggest that collagen can activate proteine kinase C, independently of the initial PIP2 breakdown.
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Fox, J. E. B., C. C. Reynolds, J. K. Boyles, R. A. Abel, and M. M. Johnson. "IDENTIFICATION OF GLYCOPROTEIN Ib8 AS THE Mr = 24,000 PLATELET POLYPEPTIDE PHOSPHORYLATED BY AGENTS THAT ELEVATE CYCLIC AMP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642926.

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Platelet function is inhibited by agents that elevate intracellular cyclic AMP concentrations, presumably as a result of the cyclic AMP-stimulated phosphorylation of intracellular proteins. Polypeptides that become phosphorylated are of Mr = 250,000, Mr = 51.000 (P51), Mr = 36,000 (P36), Mr = 24,000 (P24), and Mr = 22.000 (P22). The Mr = 250,000 polypeptide is actin-binding protein, but the identity of the other polypeptides 1s unknown. In the present study, we identified the P24 polypeptide. Platelets were radiolabeled with [32P]P1 and then Incubated for 2-5 min in the presence or absence of 5 μM prostaglandin E1 (PGE1). The PGE1-induced phosphorylation of P24 was detected on autoradiograms of SDS-gels. Since P24 has been shown to be membrane-associated, its molecular weight was compared with those of known membrane proteins. P24 comigrated with the β-chain of purified GP Ib on reduced gels (Mr = 24,000) and also on nonreduced gels (when GP Ibβ is disulfide-linked to GP Ibα and migrates with Mr = 170,000). Like GP Ibβ, P24 was associated with actin filaments in Triton X-100 lysates. Both GP Ibβ and P24 were selectively associated with filaments of the membrane skeleton and were released from filaments when the Ca2+-dependent protease was active. Antibodies against GP Ib immunoprecipitated P24 from platelet lysates. Finally, exposure of Bernard-Soulier platelets (that lacked GP Ib) to PGE1 resulted in phosphorylation of actin-binding protein, P51, P36, and P22, but not P24. We conclude that P24 is GP Ibβ. To determine whether phosphorylation of GP Ibβ is responsible for the inhibitory effects of PGE1 on platelets, we compared the action of PGE1 on control platelets with that on Bernard-Soulier platelets. One of the ways in which PGE1 inhibits platelet activation is by inhibiting the polymerization of actin. While PGE1 inhibited actin polymerization in control platelets, it did not in Bernard-Soulier platelets. We conclude that GP Ibβ is phosphorylated by agents that elevate cyclic AMP and that phosphorylation of this glycoprotein results in inhibition of platelet function.
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Reports on the topic "ProteÃna p53"

1

Chen, Junjie, and Anindya Dutta. Cellular Proteins Interacting with the Tumor Suppressor Protein p53. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada333509.

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Chen, Junjie. Cellular Proteins Interacting with the Tumor Suppressor Protein p53. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada305736.

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Chen, Junjie. Cellular Proteins Interacting with the Tumor Suppressor Protein p53. Fort Belvoir, VA: Defense Technical Information Center, August 1996. http://dx.doi.org/10.21236/ada316821.

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Wang, Bin, and Stephen J. Elledge. Involvement of 53BP1, a p43 Binding Protein, in Chk2 Phosphorylation of p53 and DNA Damage Cell Cycle Checkpoints. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417278.

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

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

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

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Dutta, Anindya. Interaction of the Tumor Suppressor p53 with Replication Protein A. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada303827.

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Dutta, Anindya. Interaction of the Tumor Suppressor p53 With Replication Protein A. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada366910.

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Dutta, Anindya. Interaction of the Tumor Suppressor p53 With Replication Protein A. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada333222.

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