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Wyszukujesz frazę "Brzóska, Kamil" wg kryterium: Autor


Wyświetlanie 1-3 z 3
Tytuł:
Iron-sulfur cluster proteins: electron transfer and beyond
Autorzy:
Brzóska, Kamil
Męczyńska, Sylwia
Kruszewski, Marcin
Powiązania:
https://bibliotekanauki.pl/articles/1041158.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
IRP1 protein
labile iron pool
aconitase
DNA glycosylases
Opis:
Iron-sulfur clusters-containing proteins participate in many cellular processes, including crucial biological events like DNA synthesis and processing of dioxygen. In most iron-sulfur proteins, the clusters function as electron-transfer groups in mediating one-electron redox processes and as such they are integral components of respiratory and photosynthetic electron transfer chains and numerous redox enzymes involved in carbon, oxygen, hydrogen, sulfur and nitrogen metabolism. Recently, novel regulatory and enzymatic functions of these proteins have emerged. Iron-sulfur cluster proteins participate in the control of gene expression, oxygen/nitrogen sensing, control of labile iron pool and DNA damage recognition and repair. Their role in cellular response to oxidative stress and as a source of free iron ions is also discussed.
Źródło:
Acta Biochimica Polonica; 2006, 53, 4; 685-691
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Nonhomologous end-joining deficiency of L5178Y-S cells is not associated with mutation in the ABCDE autophosphorylation cluster
Autorzy:
Brzóska, Kamil
Kruszewski, Marcin
Szumiel, Irena
Powiązania:
https://bibliotekanauki.pl/articles/1041297.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mouse lymphoma L5178Y
nonhomologous end-joining
autophosphorylation
DNA-dependent protein kinase
double strand break repair
Opis:
Cells with mutated autophosphorylation sites in the ABCDE cluster of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are defective in the repair of ionising radiation-induced DSB, but show in an in vitro test the same DNA-PK activity as the cells possessing wild type enzyme. Nevertheless, the mutated DNA-PK is able to undergo ATP-dependent autophosphorylation and inactivation. This characteristics correspond well with the phenotypic features of the L5178Y-S (LY-S) cell line that is defective in DSB repair, shows a pronounced G1 phase radiosensitivity, but in which the level of DNA-PK activity present in total cell extracts is similar to that of its radioresistant counterpart L5178Y-R (LY-R) cell line. The purpose of this work was to examine the possible alterations in the sequence encoding the cluster of autophosphorylation sites in the DNA-dependent protein kinase in LY-S cells. Despite the presence of phenotypic features indicating the possibility of such alterations, no differences were found between the sequences coding for the autophosphorylation sites in L5178Y-R and L5178Y-S cells. In conclusion, the repair defect in LY-S cells is not related to the structure of the DNA-PK autophosphorylation sites (ABCDE casette).
Źródło:
Acta Biochimica Polonica; 2006, 53, 1; 233-236
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity
Autorzy:
Siomek, Agnieszka
Brzoska, Kamil
Sochanowicz, Barbara
Gackowski, Daniel
Rozalski, Rafal
Foksinski, Marek
Zarakowska, Ewelina
Szpila, Anna
Guz, Jolanta
Bartlomiejczyk, Teresa
Kalinowski, Bartlomiej
Kruszewski, Marcin
Olinski, Ryszard
Powiązania:
https://bibliotekanauki.pl/articles/1042730.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Cu,Zn-SOD deficiency
NF-κB pathway
oxidative stress
Opis:
Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 577-583
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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