Temat: p53 - Katalog OPAC zbiorów

Skocz do pozycji: 1.

Tytuł:: The Reformation of Turkish Commercial Law within the Process of European Union Candidacy
Autorzy:: Yasan, Mustafa
Powiązania:: https://bibliotekanauki.pl/articles/915234.pdf
Data publikacji:: 2020
Wydawca:: Katolicki Uniwersytet Lubelski Jana Pawła II
Tematy:: Turkish commercial law, Turkish Code of Commerce, Turkey EU relations, Turkish company law.
Abuzer Kendigelen, 2016, Türk Ticaret Kanunu Değişiklikler, Yenilikler ve İlk Tespitler, 3. Baskı, İstanbul, Oniki Levha Yayınları. Ali Bozer / Celal Göle, 2018, Kıymetli Evrak Hukuku, 8. Baskı, Ankara, Banka ve Ticaret Hukuku Araştırma Enstitüsü Yayınları. Ali Bozer / Celal Göle, 2018, Ticari İşletme Hukuku, 5. Baskı, Ankara, Banka ve Ticaret Hukuku Araştırma Enstitüsü Yayınları. Alihan Aydın, 2012, Ticari İşletme Kavramı, Unsurları ve Hukuki İşlemlere Konu Olması, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.9-21, İstanbul. Arslan Kaya, 2012, Acentelik ile İlgili Yenilikler, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.53-71, İstanbul. Burak Sertoğlu, 2019, Ticari İşletme Devri, Ankara, Seçkin Yayınevi. Enver Bozkurt / Arif Köktaş, Avrupa Birliği Hukuku, 2018, 7. Baskı, Ankara, Legem Yayıncılık. Erdoğan Moroğlu, 2012, 6102 sayılı Türk Ticaret Kanunu, Değerlendirmeler ve Öneriler, 7. Baskı, İstanbul, Oniki levha Yayınları. Hamdi Yasaman, 2012, Haksız Rekabet, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.33-46, İstanbul. Hikmet Sami Türk, 2005, Tasarı Hakkında Genel Değerlendirme, Türk Ticaret Kanunu Tasarısı, Konferans, p.17-41, Ankara. Mehmet Bahtiyar, 2013, Kıymetli Evrak Hukuku, 11. Bası, İstanbul, Beta Yayınevi. Mehmet Bahtiyar, 2019, Ortaklıklar Hukuku, 13. Bası, İstanbul, Beta Yayınevi. Mehmet Emin Bilge, 1999, Ticaret Sicili, İstanbul, Beta Yayınevi. Mehmet Fatih Arıcı, 2008, Ticari İşletmenin Aktif ve Pasifi ile Devri, İstanbul, Vedat Kitapçılık. Mustafa Çeker, 2013, Ticaret Hukuku, 6. Baskı, Adana, Karahan Kitapevi. Oğuz İmregün, 1996, Kara Ticaret Hukuku Dersleri, 11. Baskı, İstanbul, Filiz Kitapevi. Oruç Hami Şener, 2016, Ticari İşletme Hukuku, Ankara, Seçkin Yayınevi. Oruç Hami Şener, 2017, Limited Ortaklıklar, Ankara, Seçkin Yayınevi. Rıza Ayhan / Mehmet Özdamar / Hayrettin Çağlar, 2012, Ticari İşletme Hukuku, 5. Bası, Ankara, Yetkin Yayınevi. Sıtkı Anlam Altay, 2012, Ticari Kayıtlar ve Defterlerin Tutulmasına İlişkin Hukuki Esaslar ve İsbat Sorunu, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.100-111, İstanbul. Şükrü Yıldız, 2012, Gerçek Kişilerde Tacir Sıfatının Kazanılması, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.21-33, İstanbul. Şükrü Yıldız, 2007, Limited Şirketler Hukuku, İstanbul, Arıkan Kitapevi. Tolga Ayoğlu, 2012, Bağlı ve Bağımsız Tacir Yardımcıları, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.46-53, İstanbul. Ünal Tekinalp, 2005, Tasarının Takdimi, Türk Ticaret Kanunu Tasarısı, Konferans, p.7-17, Ankara. Veliye Yanlı, 2012, Ticaret Sicili, Yeni Türk Ticaret Kanunu’nun Ticari İşletme Hukuku Alanında Getirdiği Yenilikler, p.89-100, İstanbul.
Opis:: The relationship between Turkey and the European Union began in 1959 with Turkey's application for membership. This relationship has survived to this day and in this process negotiations for membership have been frozen. This process contributed directly to Turkish law. This contribution has become more significant, especially since 1999. Turkish Code of Commerce entered into force in 2012, is recognized as a result of Turkey's EU process. By this Code, it is aimed to ensure harmonization between Turkish Commercial Law and EU legislation. For this reason, regulations in the sense of reform were included in TCC. However, the Code has been amended for a total of eighteen times. Sixteen times after the coming into force, two times even before coming into force. More than three hundred articles have been directly affected by these changes. The principles foreseen in the Code have been abandoned because of adopting a populist approach. This situation is accepted as a failure and disappointment for the TCC codification experience.
Źródło:: Review of European and Comparative Law; 2020, 40, 1; 25-43
2545-384X
Pojawia się w:: Review of European and Comparative Law
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Quantitative analysis of the level of p53 and p21WAF1 mRNA in human colon cancer HT-29 cells treated with inositol hexaphosphate
Autorzy:: Węglarz, Ludmiła
Molin, Izabela
Orchel, Arkadiusz
Parfiniewicz, Beata
Dzierżewicz, Zofia
Powiązania:: https://bibliotekanauki.pl/articles/1041248.pdf
Data publikacji:: 2006
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: p21WAF1
inositol hexaphosphate
RT-PCR
HT-29 cells
p53
Opis:: The aim of this study was to analyze the molecular mechanism of inositol hexaphosphate (InsP6) action through which it may inhibit proliferation of colon cancer cells and cell cycle progression. A kinetic study of p53 and p21WAF1 mRNA increase was performed on human colon cancer HT-29 cells after treatment with 1, 5 and 10 mM InsP6 for 6, 12, 24 and 48 h. Real-time-QPCR based on TaqMan methodology was applied to analyze quantitatively the transcript levels of these genes. The transcription of β-actin and GAPDH genes was assessed in parallel to select the control gene with least variability. The 2-ΔΔCt method was used to analyze the relative changes in gene transcription. InsP6 stimulated p53 and p21WAF1 expression at the mRNA level, with the highest increase in p21WAF1 mRNA occurring at 24 h, i.e., following the highest increase in p53 mRNA observed at 12 h. Based on these studies it may be concluded that the ability of InsP6 to arrest the cell cycle may be mediated by the transcriptional up-regulation of the p53-responsive p21WAF1 gene.
Źródło:: Acta Biochimica Polonica; 2006, 53, 2; 349-356
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 3.

Tytuł:: Changes in phosphorylation of histone H2A.X and p53 in response of peripheral blood lymphocytes to gamma irradiation
Autorzy:: Vilasová, Zdeňka
Řezáčová, Martina
Vávrová, Jiřina
Tichý, Aleš
Vokurková, Doris
Zoelzer, Friedo
Řeháková, Zuzana
Osterreicher, Jan
Lukášová, Emilie
Powiązania:: https://bibliotekanauki.pl/articles/1040760.pdf
Data publikacji:: 2008
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: lymphocyte
ionizing radiation
p53
phytohemagglutinin (PHA)
apoptosis
DNA damage
Opis:: The main aim of this study was to compare the reaction of quiescent and proliferating, i.e. phytohemagglutinin (PHA)-stimulated, human peripheral blood mononuclear cells (PBMCs) to γ-radiation, and analyse changes of proteins related to repair of DNA damage and apoptosis, such as γH2A.X, p53, p53 phosphorylation at serines-15 and -392, and p21 and their dose dependence. Freshly isolated PBMCs in peripheral blood are predominantly quiescent, in G0 phase, and with very low amounts of proteins p53 and p21. Using confocal microscopy we detected dose dependent (0.5-5 Gy) induction of foci containing γH2A.X (1 h after γ-ray exposure), which are formed around radiation-induced double strand breaks of DNA. Apoptosis was detected from 24 h after irradiation by the dose of 4 Gy onwards by Annexin V binding and lamin B cleavage. Seventy two hours after irradiation 70% of CD3+ lymphocytes were A+. Neither increase in p53 nor its phosphorylation on serine-392 after irradiation was detected in these cells. However, massive increase in p21 (cyclin-dependent kinase inhibitor 1A) was detected after irradiation, which can be responsible for late occurrence of apoptosis in these quiescent cells. PHA-stimulation itself (72 h) caused an increase in early apoptosis (A+PI-) in comparison to non-stimulated PBMCs (38% A+ resp. 13.4%). After PHA-stimulation also the amount of γH2A.X, p53, and p21 increased, but no phosphorylation of p53 on serine-392 or -15 was detected. Reaction to γ-radiation was different in PHA-stimulated lymphocytes: the p53 pathway was activated and p53 was phosphorylated on serines-15 and -392 4 h after irradiation by the dose of 4 Gy. Phosphorylation of p53 at serine-15 increased in a dose-dependent manner in the studied dose range 0.2-7.5 Gy. Also the amount of p21 increased after irradiation. Seventy two hours after irradiation of PHA-stimulated CD3+ T lymphocytes by the dose of 4 Gy 65% of cells were A+.
Źródło:: Acta Biochimica Polonica; 2008, 55, 2; 381-390
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 4.

Tytuł:: The effect of phenobarbital on gene expression levels of p53 and DNMT1 in the liver of Wistar rats
Autorzy:: Urbanek-Olejnik, K.
Liszewska, M.
Kostka, G.
Powiązania:: https://bibliotekanauki.pl/articles/874211.pdf
Data publikacji:: 2014
Wydawca:: Narodowy Instytut Zdrowia Publicznego. Państwowy Zakład Higieny
Tematy:: phenobarbital
gene expression
animal exposure
rat
p53 gene
Dnmt1 gene
liver
Wistar rat
Opis:: Background. Our previous studies have shown that short-term treatment with phenobarbital (PB) resulted in cytosine methylation of CpG sites on the p53 gene promoter in male Wistar rats’ liver. Furthermore, PB induced DNA-methyltransferases (DNMTs) activity was also demonstrated; being the enzymes that catalyze methyl group transfer to cytosine in CpG dinucleotides. Objective. Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes. Material and methods. Male Wistar rats received PB in three daily oral doses (at 24-h intervals) of 92,8 mg/kg b.w. x day-1. Levels of mRNA for p53 and Dnmt1 and levels of relevant proteins were respectively examined by Real-Time PCR and Western blot analysis. Results. Gene expression analysis revealed that exposure of Wistar rats to PB caused statistically significant alternations in the expression of tested genes. We found that both mRNA and protein expression of p53 was down-regulated, whereas expression of Dnmt1 (both mRNA and protein) was up-regulated after PB treatment. Conclusions. Suppression of p53 mRNA and protein expression, which is probably a result of epigenetic changes, (in particular aberrant p53 promoter hypermethylation), can be associated with tumour promoting activity of phenobarbital.
Wprowadzenie. Nasze wcześniejsze badania wykazały, że krótkoterminowe narażenie szczurów Wistar na fenobarbital (PB) stymulowało metylację cytozyny w badanych sekwencjach rejonu promotorowego genu p53. Ponadto stwierdzono wzrost aktywności metylotransferaz DNA (DNMT), enzymów które katalizują przenoszenie grupy metylowej do cytozyny w dinukleotydach CpG. Cel badań. Z uwagi że metylacja DNA pełni istotną rolę w ekspresji genów, a DNMT1 uczestniczy w regulacji metylacji DNA, w prezentowanych badaniach oceniano czy indukowana PB hipermetylacja rejonu promotorowego genu p53 była związana ze zmianami ekspresji genów p53 i Dnmt1. Materiał i metody. Samce szczurów szczepu Wistar otrzymywały PB w dawce 92,8 mg/kg m.c. x dzień-1, 3-krotnie w odstępach dobowych. Analizę poziomu transkryptów i białek badanych genów przeprowadzano odpowiednio metodą Real- -Time PCR i Western blot. Wyniki. W wyniku oddziaływania PB wykazano obniżoną ekspresję genu p53 i wzrost ekspresji metylotranserazy 1 (DNMT1). Wnioski. Supresja ekspresji p53 (na poziomie mRNA i białka) będąca prawdopodobnie wynikiem zmian epigenetycznych, w szczególności hipermetylacji jego rejonu promotorowego może być związana z promocyjną aktywnością fenobarbitalu.
Źródło:: Roczniki Państwowego Zakładu Higieny; 2014, 65, 3
0035-7715
Pojawia się w:: Roczniki Państwowego Zakładu Higieny
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 5.

Tytuł:: Wpływ ftalanu dibutylu (DBP) na poziom metylacji i ekspresji genu p53 w wątrobie szczurów Wistar
The effect of dibutyl phthalate (DBP) on the methylation and expression level of p53 gene in the liver of Wistar rats
Autorzy:: Urbanek-Olejnik, K
Liszewska, M
Kostka, G
Powiązania:: https://bibliotekanauki.pl/articles/872276.pdf
Data publikacji:: 2012
Wydawca:: Narodowy Instytut Zdrowia Publicznego. Państwowy Zakład Higieny
Tematy:: ftalan dibutylu
dzialanie rakotworcze
toksycznosc
szczury
watroba
metylacja
ekspresja genow
gen p53
Opis:: Wprowadzenie. Indukowane niegenotoksycznymi kancerogenami (NGCs) zmiany metylacji DNA rozpatrywane są jako mechanizm ich toksycznego, w tym rakotwórczego działania. Cel badań. Celem podjętych badań była ocena statusu metylacji rejonu promotorowego i ekspresji genu p53 na poziomie mRNA oraz białka w wyniku oddziaływania ftalanu dibutylu (DBP). Badania zmierzały do oceny zależności pomiędzy ekspresją genu p53 a poziomem metylacji jego rejonu promotorowego. Materiał i metody. Samce szczurów szczepu Wistar otrzymywały DBP w dawce 1800 mg/kg m.c. x dzień-1 jednorazowo, 3-krotnie i 14-krotnie. Ocenę stopnia zmian metylacji badanych sekwencji CpG rejonu promotorowego genu p53 dokonano metodą MSRA (ang. Methylation-Sensitive Restriction Enzyme Analysis). Analizę względnego poziomu transkryptów badanego genu przeprowadzano metodą PCR w czasie rzeczywistym natomiast ocenę ekspresji genu na poziomie białka - techniką Western Blot. Wyniki. W wyniku oddziaływania DBP wykazano wzrost metylacji genu p53 po jednorazowym narażeniu zwierząt badanym związkiem. Nie stwierdzono bezpośredniej zależności pomiędzy poziomem ekspresji genu p53 a metylacją badanych sekwencji rejonu promotorowego genu p53. Obniżony poziom białka p53 obserwowano przez cały okres doświadczalny. Wnioski. Wykazano brak zależność pomiędzy poziomem ekspresji genu p53 a zmianami metylacji jego rejonu promotorowego. Obniżony poziom białka p53, był prawdopodobnie efektem represyjnego oddziaływania białka c-myc, uczestniczącego w tych samych szlakach transdukcji sygnału.
Background. Currently, nongenotoxic carcinogens-induced changes in DNA methylation profile are considered as mechanism of their toxicity, including carcinogenic action. Objective. The aim of the study was to determine the effect of dibutyl phthalate (DBP) on the methylation levels of the p53 promoter region, as well as mRNA and protein level of this gene. Material and method. Male Wistar rats received DBP in one, three or fourteen daily oral doses (at 24-h intervals) of 1800 mg/kg b.w. x day-1. The methylation level of c-myc gene was determined by PCR-based methylation sensitive restriction enzyme analysis (MSRA). The expression of gene was assessed by Real-Time PCR (at mRNA level) and Western blot (at protein level) analysis. Results. There was observed the hypermethylation of p53 promoter region after short (1 day) exposure of the animals to DBP. No correlation was found between mRNA expression and methylation level of p53 gene. The present study showed decreased level of p53 protein, during the whole period of study. Conclusions. No direct correlation was observed between the methylation and expression level of p53. The decreased protein level might be a consequence of the repressive effect of c-myc, which was involved in signal transduction pathways, the same as p53 protein.
Źródło:: Roczniki Państwowego Zakładu Higieny; 2012, 63, 4
0035-7715
Pojawia się w:: Roczniki Państwowego Zakładu Higieny
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 6.

Tytuł:: Gamma-radiation-induced ATM-dependent signalling in human T-lymphocyte leukemic cells, MOLT-4
Autorzy:: Tichý, Aleš
Záškodová, Darina
Řezáčová, Martina
Vávrová, Jiřina
Vokurková, Doris
Pejchal, Jaroslav
Vilasová, Zdena
Cerman, Jaroslav
Österreicher, Jan
Powiązania:: https://bibliotekanauki.pl/articles/1041075.pdf
Data publikacji:: 2007
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: checkpoint kinase-2
ionizing radiation
p53
ATM kinase
Mdm2
Opis:: ATM kinase (ATM) is essential for activation of cell cycle check points and DNA repair in response to ionizing radiation (IR). In this work we studied the molecular mechanisms regulating DNA repair and cell death in human T-lymphocyte leukemic cells, MOLT-4. Apoptosis was evaluated by flow-cytometric detection of annexin V. Early apoptotic cells were determined as sub-G1 cells and late apoptotic cells were determined as APO2.7-positive ones. Proteins involved in ATM signalling pathway were analysed by Western-blotting. We observed a rapid (0.5 h) phosphorylation of ATM declining after 6 h after irradiation by all the doses studied (1.5, 3.0, and 7.5 Gy). Checkpoint kinase-2 (Chk-2) was also phosphorylated after 0.5 h but its phosphorylated form persisted 4, 2, and 1 h after the doses of 1.5, 3.0, and 7.5 Gy, respectively. The amount of p53 protein and its form phosphorylated on Ser-392 increased 1 h after irradiation (1-10 Gy). The lethal dose of 7.5 Gy caused an immediate induction and phosphorylation of p53 after 0.5 h post-irradiation. At the time of phosphorylation of p53, we found simultaneous phosphorylation of the oncoprotein Mdm2 on Ser-166. Neither ATM nor its downstream targets showed a dose-dependent response after 1 h when irradiated by the doses of 1-10 Gy. MOLT-4 cells were very sensitive to the effect of IR. Even low doses, such as 1.5 Gy, induced apoptosis 16 h after irradiation (evaluated according to the cleavage of nuclear lamin B to a 48-kDa fragment). IR-induced molecular signalling after exposure to all the tested doses was triggered by rapid phosphorylation of ATM and Chk-2. Subsequent induction of p53 protein and its phosphorylation was accompanied by concomitant phosphorylation of its negative regulator, oncoprotein Mdm2, and followed by induction of apoptosis.
Źródło:: Acta Biochimica Polonica; 2007, 54, 2; 281-287
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 7.

Tytuł:: The role of the 5 terminal region of p53 mRNA in the p53 gene expression
Autorzy:: Swiatkowska, Agata
Zydowicz, Paulina
Sroka, Joanna
Ciesiołka, Jerzy
Powiązania:: https://bibliotekanauki.pl/articles/1038716.pdf
Data publikacji:: 2016
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: p53
transcription
translation
non-coding region
mRNA
IRES
Opis:: The p53 tumour suppressor protein is one of the major factors responsible for cell cycle regulation and protection against cancer development. This is why it is often referred to as "the guardian of the genome". On the other hand, mutations in the p53 gene are connected with more than 50% of tumours of various types. The thirty-six years of extensive research on the p53 gene and its protein products have shown how sophisticated the p53-based cell system control is. An additional level of complexity of the p53 research is connected with at least twelve p53 isoforms which have been identified in the cell. Importantly, disturbance of the p53 isoforms' expression seems to play a key role in tumorigenesis, cell differentiation and cell response to pathogenic bacteria, and RNA and DNA viruses. Expression of various p53 isoforms results from the usage of different transcription promoters, alternative splicing events and translation initiation from alternative AUG codons. The importance of the 5'-terminal regions of different p53 mRNA transcripts in the multi-level regulation of the p53 gene has recently been documented. In this review we focus on the structural features of these regions and their specific role in the p53 translation initiation process.
Źródło:: Acta Biochimica Polonica; 2016, 63, 4; 645-651
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 8.

Tytuł:: Effect of aging and oxidative/genotoxic stress on poly(ADP-ribose) polymerase-1 activity in rat brain
Autorzy:: Strosznajder, Robert
Jesko, Henryk
Adamczyk, Agata
Powiązania:: https://bibliotekanauki.pl/articles/1041342.pdf
Data publikacji:: 2005
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: aging
poly(ADP-ribosyl)ation
brain
p53 protein
PARP-1
genotoxic stress
oxidative stress
Opis:: Poly(ADP-ribose) polymerase-1 (PARP-1, EC 2.4.2.30), a DNA-bound enzyme, plays a key role in genome stability, but after overactivation can also be responsible for cell death. The aim of the present study was to investigate PARP-1 activity in the hippocampus, brain cortex, striatum and cerebellum in adult (4 months) and aged (24 months) specific pathogen free Wistar rats and to correlate it with PARP-1 protein level and p53 expression. Moreover, the response of PARP-1 in adult and aged hippocampus to oxidative/genotoxic stress was evaluated. Our data indicated a statistically significant enhancement of PARP-1 activity in aged hippocampus and cerebral cortex comparing to adults without statistically significant changes in PARP-1 protein level. The expression of p53 mRNA was elevated in all aged brain parts with the exception of the cerebral cortex. Our data suggest that enhancement of PARP-1 activity and p53 expression in aged brain may indicate higher DNA damage. Our data also indicate that during excessive oxidative/genotoxic stress there is no response of PARP-1 activity in aged hippocampus in contrast to a significant enhancement of PARP-1 activity in adults which may have important consequences for the physiology and pathology of the brain.
Źródło:: Acta Biochimica Polonica; 2005, 52, 4; 909-914
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 9.

Tytuł:: Prospects for p53-based cancer therapy.
Autorzy:: Stokłsa, Tomasz
Gołąb, Jakub
Powiązania:: https://bibliotekanauki.pl/articles/1041406.pdf
Data publikacji:: 2005
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: missense mutations
cancer
p53
stress response
small molecule inhibitors
tumor suppressor
Opis:: The p53 tumor suppressor plays the role of a cellular hub which gathers stress signals such as damage to DNA or hypoxia and translates them into a complex response. p53 exerts its action mainly as a potent transcription factor. The two major outcomes of p53 activity are highlighted: cell cycle arrest and apoptosis. During malignant transformation p53 or p53-pathway related molecules are disabled extremely often. Mutations in p53 gene are present in every second human tumor. A mutant form of p53 may not only negate the wild type p53 function but may play additional role in tumor progression. Therefore p53 represents a relatively unique and specific target for anticancer drug design. Current approaches include several different molecules able to restore p53 wild-type conformation and activity. Such small molecule drugs hold great promise in treating human tumors with dysfunction of p53 pathway in the near future.
Źródło:: Acta Biochimica Polonica; 2005, 52, 2; 321-328
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 10.

Tytuł:: Family with Li-Fraumeni syndrome and no evidence of a germline mutation of the p53 gene or chromosomal aberrations
Autorzy:: Sikorska, A
Traczyk, Z.
Konopka, L.
Fiszer-Maliszewska, L.
Wojciechowska, B.
Pienkowska-Grela, B.
Rygier, J.
Woroniecka, R.
Witkowska, A.
Rusin, M.
Powiązania:: https://bibliotekanauki.pl/articles/2041808.pdf
Data publikacji:: 2001
Wydawca:: Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:: germline mutation
Li-Fraumeni syndrome
brain tumour
carcinoma
child
chromosome aberration
cancer
p53 gene
young adult
Źródło:: Journal of Applied Genetics; 2001, 42, 3; 379-384
1234-1983
Pojawia się w:: Journal of Applied Genetics
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 11.

Tytuł:: Advantage of a baculovirus expression system for protein-protein interaction studies. Involvement of posttranslational phosphorylation in the interaction between wt p53 protein and poly(ADP-ribose) polymerase-1
Autorzy:: Schmid, Gerald
Wojciechowski, Jacek
Węsierska-Gądek, Józefa
Powiązania:: https://bibliotekanauki.pl/articles/1041382.pdf
Data publikacji:: 2005
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: nucleocytoplasmic shuttling
NES
p53 isomers
p53 stability
cell cycle arrest
2D-PAGE
p53 nuclear export
FACS analysis
p53 pull-down assay
p53 phosphorylation
Opis:: We recently observed an interaction between poly(ADP-ribose) polymerase-1 (PARP-1) and the tumor suppressor p53 protein. However, more extensive studies on both proteins, especially those on characterization of their domains involved in the interaction were difficult due to very low expression levels of p53 in mammalian cells. Therefore, we generated recombinant proteins for such studies. To clarify which domains of human PARP-1 and of human wild-type (wt) p53 were involved in this protein-protein interaction, we generated baculoviral constructs encoding full length or distinct functional domains of both proteins. Full length PARP-1 was simultaneously coexpressed in insect cells with full length wt p53 protein or its distinct truncated fragments and vice versa. Reciprocal immunoprecipitation of Sf9 cell lysates revealed that the central and carboxy-terminal fragments of p53 each were sufficient to confer binding to PARP-1, whereas the amino-terminal part harbouring the transactivation functional domain was dispensable. On the other hand, the amino-terminal and central fragments of PARP-1 were both necessary for complex formation with p53 protein. Since the most important features of p53 protein are regulated by phosphorylation, we addressed the question whether its phosphorylation is essential for the binding between the two proteins. Baculovirally expressed wt p53 was post-translationally modified. At least six distinct p53 isomers were resolved by immunoblotting following two-dimensional separation of baculovirally expressed wt p53 protein. Using specific phospho-serine antibodies, we identified phosphorylation of baculovirally expressed p53 protein at five distinct sites. To define the role of p53 phosphorylation, pull-down assays using untreated and dephosphorylated p53 protein were performed. Dephosphorylated p53 failed to bind PARP-1, indicating that complex formation between the two proteins was regulated by phosphorylation of p53. The marked phosphorylation of p53 at Ser392 observed in unstressed cells suggests that the phosphorylated carboxy-terminal part of p53 undergoes complex formation with PARP-1 resulting in masking of the NES and thereby preventing its export.
Źródło:: Acta Biochimica Polonica; 2005, 52, 3; 713-719
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 12.

Tytuł:: Rola komórek macierzystych w etiopatogenezie nowotworów ośrodkowego układu nerwowego
Autorzy:: Rieske, Piotr
Powiązania:: https://bibliotekanauki.pl/articles/1061281.pdf
Data publikacji:: 2006
Wydawca:: Medical Communications
Tematy:: APC
P53
SHH
WNT
tumor stem cells
nowotworowe komórki macierzyste
Opis:: The paper presents current views concerning the role of stem cells in neoplasia, with particular emphasis of CNS tumors. First, some arguments are presented supporting the thesis that at the first stage of neoplasia, the cellular target for carcinogens are normal stem cells or progenitor cells. Also, discussed are important problems associated with attempts at identification of cellular sources of neoplasms. One of these is the difficulty encountered with distinguishing stem cells and non-differentiated cells. Second, data are presented allowing the conclusion that within neoplastic tissue exist neoplastic stem cells - cells enabling regeneration of this pathological tissue. In the context of discussion concerning the role of stem cells in the pathogenesis of neoplasms, a new theory about physiologic and pathologic role of normal and damaged proteins, e.g. APC, SUFU, EGFR, c-MYC, P53 is presented. Discussed is also the role of proteins controlling modification of chromatin, e.g. the Polycomb protein. These proteins are extremely important for the differentiation process. The paper presents also own preliminary experience with the role of stem cells in the pathogenesis of CNS tumors. Finally, presented are premises providing hope for application of knowledge concerning neoplastic stem cells in designing novel modalities of oncologic therapies. Development of such therapies may be based on the search for chemotherapeutic agents which would selectively eliminate neoplastic stem cells. It is also possible to use normal but genetically modified stem cells to detect neoplastic stem cells and to eliminate them.
W artykule przedstawiono aktualne poglądy na temat udziału komórek macierzystych w nowotworzeniu, ze szczególnym uwzględnieniem nowotworów ośrodkowego układu nerwowego. Po pierwsze przytoczono niektóre argumenty na rzecz tezy, iż komórkowym celem dla karcynogenów na pierwszym etapie nowotworzenia są prawidłowe komórki macierzyste lub komórki progenitorowe. Jednocześnie omówiono istotne problemy, z jakimi wiążą się próby identyfikacji komórkowego źródła nowotworów. Jednym z nich jest problem odróżnienia komórek macierzystych od komórek zróżnicowanych. Po drugie zaprezentowano dane pozwalające stwierdzić, iż w obrębie tkanki nowotworowej bytują komórki macierzyste nowotworu – komórki umożliwiające regenerację tej patologicznej tkanki. W kontekście rozważań dotyczących roli komórek macierzystych w etiopatogenezie nowotworów przedstawiono nową teorię na temat fizjologicznej i patologicznej roli pełnionej przez prawidłowe i uszkodzone białka, takie jak APC, SUFU, EGFR, c-MYC, P53. Omówione także udział w nowotworzeni, białek kontrolujących modyfikację chromatyny jak np. białka Polycomb. Białka te odgrywają niezwykle istotną rolę w czasie różnicowania. W artykule omówiono także pierwsze doświadczenie własne związane z udziałem komórek macierzystych w etiopatogenezie nowotworów OUN. Wreszcie przedstawione zostały przesłanki dające nadzieję na wykorzystanie wiedzy o nowotworowych komórkach macierzystych do projektowania nowych rodzajów terapii przeciwnowotworowej. Opracowywanie tych terapii może być oparte na poszukiwaniu chemioterapeutyków selektywnie eliminujących nowotworowe komórki macierzyste. Możliwe jest również wykorzystanie prawidłowych, ale zmodyfikowanych genetycznie komórek macierzystych do wyśledzenia nowotworowych komórek macierzystych i ich eliminacji.
Źródło:: Aktualności Neurologiczne; 2006, 6, 3; 169-174
1641-9227
2451-0696
Pojawia się w:: Aktualności Neurologiczne
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 13.

Tytuł:: Regulation of p53 by siRNA in radiation treated cells: Simulation studies
Autorzy:: Puszyński, K.
Jaksik, R.
Świerniak, A.
Powiązania:: https://bibliotekanauki.pl/articles/331259.pdf
Data publikacji:: 2012
Wydawca:: Uniwersytet Zielonogórski. Oficyna Wydawnicza
Tematy:: siRNA
p53
terapia skojarzona
combined therapy
Opis:: Ionizing radiation activates a large variety of intracellular mechanisms responsible for maintaining appropriate cell functionality or activation of apoptosis which eliminates damaged cells from the population. The mechanism of such induced cellular death is widely used in radiotherapy in order to eliminate cancer cells, although in some cases it is highly limited by increased cellular radio-resistance due to aberrations in molecular regulation mechanisms of malignant cells. Despite the positive correlation between the radiation dose and the number of apoptotic cancer cells, radiation has to be limited because of extensive side effects. Therefore, additional control signals whose role will be to maximize the cancer cells death-ratio while minimizing the radiation dose and by that the potential side effects are worth considering. In this work we present the results of simulation studies showing possibilities of single gene regulation by small interfering RNA (siRNA) that can increase radio-sensitivity of malignant cells showing aberrations in the p53 signaling pathway, responsible for DNA damage-dependant apoptosis. By blocking the production of the p53 inhibitor Mdm2, radiation treated cancer cells are pushed into the apoptotic state on a level normally achievable only with high radiation doses. The presented approach, based on a simulation study originating from experimentally validated regulatory events, concerns one of the basic problems of radiotherapy dosage limitations, which, as will be shown, can be partially avoided by using the appropriate siRNA based control mechanism.
Źródło:: International Journal of Applied Mathematics and Computer Science; 2012, 22, 4; 1011-1018
1641-876X
2083-8492
Pojawia się w:: International Journal of Applied Mathematics and Computer Science
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 14.

Tytuł:: Proinflammatory cytokines (IL-6, IL-18) and apoptotic factors (HP 53, survivin) in patients with alcoholic liver cirrhosis
Autorzy:: Prystupa, Andrzej
Kiciński, Paweł
Sak, Jarosław
Grzybowski, Andrzej
Boguszewska-Czubara, Anna
Toruń-Jurkowska, Anna
Niedziałek, Jarosław
Załuska, Wojciech
Powiązania:: https://bibliotekanauki.pl/articles/972717.pdf
Data publikacji:: 2017
Wydawca:: Instytut Medycyny Wsi
Tematy:: survivin
alcoholic liver cirrhosis
proinflammatory cytokines
apoptosis
human protein p53
Opis:: Background. Apoptosis is involved in the pathogenesis of alcoholic liver cirrhosis. Its development can be triggered by an inflammatory process. In the present study, levels of apoptotic factors – survivin human protein p53 (HP 53) and IL-6, IL-18 were determined according to the stage of liver cirrhosis. Material and methods. Seventy patients with alcoholic liver cirrhosis, treated in various hospitals of the Lublin region, Poland were included in the study. Serum levels of IL-6, IL-18, HP53 and survivin were determined by the enzyme-linked immunosorbent assay (ELISA) technique. Results. The serum level of survivin in patients with alcoholic liver cirrhosis was not statistically different from that found in the control group. The level of HP53 was significantly higher in the group of patients with alcoholic liver cirrhosis compared to the control group (16.53±22.69 vs. 0.39±1.31 U/ml; p<0.001). Likewise, the level of IL-6 was significantly higher in the group of patients with alcoholic liver cirrhosis compared to the control group (33.83±41.78 vs. 0.88 ± 0.56 pg/ml; p<0.001). Moreover, the level of IL-18 was significantly higher in the group of patients with liver cirrhosis compared to the control group (23.96±31.07 vs. 5.3±8.6 pg/ml; p<0.001). Conclusion. In conclusion, increased serum levels of IL-6 and IL-18 were demonstrated in patients with alcoholic liver cirrhosis. Moreover, the liver cirrhosis patients had elevated levels of HP53, which is a marker of apoptosis. Our results did not demonstrate the correlation between the levels of apoptosis markers (survivin, HP53) and the levels of cytokines (IL-6, IL-18) in the blood serum.
Źródło:: Journal of Pre-Clinical and Clinical Research; 2017, 11, 1; 1-5
1898-2395
Pojawia się w:: Journal of Pre-Clinical and Clinical Research
Dostawca treści:: Biblioteka Nauki