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    Wyświetlanie 1-3 z 3
    Tytuł:
    Inhibition of poly(ADP-ribose) polymerase activity affects its subcellular localization and DNA strand break rejoining
    Autorzy:
    Ryabokon, Nadezhda
    Cieślar-Pobuda, Artur
    Rzeszowska-Wolny, Joanna
    Powiązania:
    https://bibliotekanauki.pl/articles/1040571.pdf
    Data publikacji:
    2009
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    DNA strand break rejoining
    efficiency of PARP inhibition
    PARP foci
    poly(ADP-ribose) polymerase (PARP)
    PARP inhibitors
    Opis:
    Poly(ADP-ribose) polymerase (PARP) plays a crucial role in DNA repair. Modulation of its activity by stimulation or inhibition is considered as a potentially important strategy in clinical practice, especially to sensitize tumor cells to chemo- and radiotherapy through inhibition of DNA repair. Here we studied the effect of the three PARP inhibitors, 5-iodo-6-amino-benzopyrone (INH2BP), 1,5-isoquinolinediol (1,5-dihydroxyisoquinolinediol (1,5-IQD) and 8-hydroxy-2-methylquinazolin-4-[3H]one (NU1025), and for two of them the efficiency in slowing the rejoining of DNA strand breaks induced by H2O2 was compared. Inhibition of PARP changed its intranuclear localization markedly; cells exposed to the inhibitor NU1025 showed a significant tendency to accumulate PARP in large foci, whereas in untreated cells its distribution was more uniform. The speed and efficiency of rejoining of H2O2-induced DNA strand breaks were lower in cells incubated with a PARP inhibitor, and the kinetics of rejoining were modulated in a different manner by each inhibitor. At a concentration of 100 µM the efficiency of the inhibitors could be ranked in the order NU1025 > IQD > INH2BP. The two first compounds were able to decrease the overall PARP activity below the level detected in control cells, while INH2BP showed up to 40% PARP activity after exposure to H2O2.
    Źródło:
    Acta Biochimica Polonica; 2009, 56, 2; 243-248
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    DNA double-strand break rejoining in radioadapted human lymphocytes: evaluation by neutral comet assay and pulse-field gel electrophoresis
    Autorzy:
    Wojewódzka, M.
    Buraczewska, I.
    Szumiel, I.
    Grądzka, I.
    Powiązania:
    https://bibliotekanauki.pl/articles/146153.pdf
    Data publikacji:
    2006
    Wydawca:
    Instytut Chemii i Techniki Jądrowej
    Tematy:
    human lymphocytes
    radioadaptation
    DNA double-strand break rejoining
    neutral comet assay
    pulsefield gel electrophoresis
    Opis:
    Adaptive response (AR), an enhanced resistance to a high dose of ionising radiation acquired after pretreatment with a very low dose, was estimated in normal human lymphocytes. The question posed was whether the extent of radioadaptation, assessed by micronucleus test, would be related to the rate of DNA double-strand break (DSB) rejoining. Phytohemagglutinin-stimulated G1-lymphocytes from 5 healthy male volunteers were pre-treated (or not) with an adaptive (5 cGy) dose of X-rays, followed by a higher (5 or 10 Gy) challenge dose after 20-22 h. DSB rejoining after the challenge dose was monitored with the use of two methods: neutral comet assay, modified to reduce the contribution of single-strand breaks (SSBs) and thermolabile sites, and pulse-field gel electrophoresis (PFGE), specific for DSBs. At the level of micronuclei, an AR was observed in lymphocytes of 3 of 5 donors. Up to 60 min, comet assay showed no statistically significant differences in DNA break rejoining between adapted and non-adapted lymphocytes, independently of AR appearance. PFGE gave similar results, although in three donors it revealed secondary increases in DSBs levels at 30 min and/or 60 min post-irradiation in the adapted vs. the non-adapted samples. Failure to demonstrate changes in DSBs rejoining rate in the adapted lymphocytes could be due to diversity of AR intensity/timing at the level of DNA repair in not fully homogenous cell populations. Also, “rare” DNA cuts characteristic of early apoptosis/necrosis could overlap the process of DNA break rejoining.
    Źródło:
    Nukleonika; 2006, 51, 4; 185-191
    0029-5922
    1508-5791
    Pojawia się w:
    Nukleonika
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Relationships between EGFR-initiated signalling, DNA double-strand break rejoining and survival in X-irradiated human glioma M059 cells
    Autorzy:
    Grądzka, I.
    Buraczewska, I.
    Szumiel, I.
    Powiązania:
    https://bibliotekanauki.pl/articles/146764.pdf
    Data publikacji:
    2008
    Wydawca:
    Instytut Chemii i Techniki Jądrowej
    Tematy:
    human glioma M059 K and J cells
    DNA-dependent protein kinase (DNA-PK)
    radiosensitivity
    DNA double-strand break (DSB) rejoining
    epidermal-growth-factor-receptor (EGFR)
    signalling inhibitors: tyrphostin
    Opis:
    The aim of this study was to investigate the effect of signalling inhibition on survival and double-strand break (DSB) rejoining in cells differing in sensitivity to inhibitors, X-rays and bleomycin. Human glioma M059 cells, K (relatively radioresistant) and J (radiosensitive, defective in DSB rejoining for lack of DNA-dependent protein kinase catalytic subunit, DNA-PKcs) were pretreated with signalling inhibitors: tyrphostin AG 1478, specific for epidermalgrowth- factor-receptor (EGFR) kinase or PD 98059, specific for kinase MEK 1/2 (mitogen-activated, extracellular signal-activated kinases 1 and 2). Subsequently, the cells were X-irradiated or treated with bleomycin. Cell survival was determined by clonogenicity test. DSB rejoining was monitored with the use of pulsed-field gel electrophoresis (PFGE). We found that in X-irradiated M059 K cells EGFR kinase activity was necessary for efficient DSB rejoining and the kinase inhibitor, tyrphostin AG 1478, acted as radiosensitizer in the dose range that reduced cell survival to 0.7-0.8. Inhibition of EGFR kinase, however, did not decrease survival or affect DSB rejoining in DNA-PKcs-deficient M059 J cells. These results indicated that the decrease in cell survival was due to a disturbed DSB rejoining by the DNA-PK dependent system. In contrast, inhibition of MEK 1/2 kinase on EGFR downstream signalling pathway by PD 98059 did not affect DSB rejoining in either cell line and exerted a radioprotective effect.
    Źródło:
    Nukleonika; 2008, 53, 2; 37-44
    0029-5922
    1508-5791
    Pojawia się w:
    Nukleonika
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-3 z 3

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