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Wyszukujesz frazę "DNA strand" wg kryterium: Temat


Wyświetlanie 1-4 z 4
Tytuł:
Histone H2AX in DNA repair
Autorzy:
Lewandowska, H.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/147030.pdf
Data publikacji:
2002
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
DNA double strand breaks
DNA repair
histone gamma-H2AX
ionising radiation
Opis:
The paper reviews the recent reports on the role of the phosphorylated histone H2AX (gamma-H2AX). The modification of this histone is an important part of the cellular response to the induction of DNA double strand breaks (DSB) by ionising radiation and other DSB-generating factors. In irradiated cell the modification is carried out mainly by ATM (ataxia- -telangiectasia mutated) kinase, the enzyme that starts the alarm signalling upon induction of DSB. gamma-H2AX molecules are formed within 1 3 min after irradiation and form foci at the sites of DSB. This seems to be necessary for the recruitment of repair factors that are later present in foci of damaged nuclei. Modification of a constant percentage of H2AX molecules per DSB takes place, corresponding to chromatin domains of megabase pairs of DNA.
Źródło:
Nukleonika; 2002, 47, 4; 127-131
0029-5922
1508-5791
Pojawia się w:
Nukleonika
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:
Concerted control of DNA double strand break repair and cell cycle progression in X-irradiated mammalian cells
Autorzy:
Sochanowicz, B.
Szumiel, I.
Powiązania:
https://bibliotekanauki.pl/articles/148697.pdf
Data publikacji:
2005
Wydawca:
Instytut Chemii i Techniki Jądrowej
Tematy:
ATM kinase
DNA double strand break repair
RAD50
cell cycle arrest
repair foci
BRCT domain
Opis:
Upon examination of cell cycle regulation in a damaged cell, relations were discovered of the cell cycle control mechanisms with a complicated web of signalling pathways, eventually called the genome surveillance system. After infliction of DNA double strand breaks (DSB), the signalling is initiated by sensor proteins and transducer protein kinase ATM. This kinase phosphorylates downstream effector proteins, such as checkpoint kinases CHK1 and CHK2, which initiate the pathways leading to cell cycle arrest. In contrast with the older model of linear transmission of signals in a certain sequence, it is now accepted that the damage signalling system is branched and contains feedback loops. DSB's presence is signalled by sensor proteins (MRE11-RAD50-nibrin complex, MRN) to ATM and the signal is amplified through adaptor proteins, MDC1/NFBD1 or 53BP1 (Tp53 binding protein). MRN contains a forkheadassociated (FHA) domain and BRCA1 carboxyl-terminal (BRCT) domain. The combination of the FHA/BRCT domains has a crucial role for the binding of nibrin to the H2AX histone, assembling the components of repair foci. These domains also are important for interaction of other proteins localised in the foci. For example, MDC1/NFBD1 contains a FHA domain and two BRCT domains which are involved in protein interactions. The signal generated at DSBs is amplified and transduced to recruit components of DNA repair systems. In a concerted way with the sequential recruitment of components of repair foci, activation of transcription of genes takes place, that is necessary for blocking progression through the cell cycle, for DNA repair or apoptosis.
Źródło:
Nukleonika; 2005, 50, 4; 129-138
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 1-4 z 4

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