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5 Acta Biochimica Polonica

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Non-homologous DNA end joining

100%

Pastwa E. , Blasiak J.

Acta Biochimica Polonica

2003

tom 50

nr 4

DNA double-strand breaks (DSBs) are a serious threat for the cell and when not repaired or misrepaired can result in mutations or chromosome rearrangements and eventually in cell death. Therefore, cells have evolved a number of pathways to deal with DSB including homologous recombination (HR), single-strand annealing (SSA) and non-homologous end joining (NHEJ). In mammals DSBs are primarily repaired by NHEJ and HR, while HR repair dominates in yeast, but this depends also on the phase of the cell cycle. NHEJ functions in all kinds of cells, from bacteria to man, and depends on the structure of DSB termini. In this process two DNA ends are joined directly, usually with no sequence homology, although in the case of same polarity of the single stranded overhangs in DSBs, regions of microhomology are utilized. The usage of microhomology is common in DNA end-joining of physiological DSBs, such as at the coding ends in V(D)J (variable(diversity) joining) recombination. The main components of the NHEJ system in eukaryotes are the catalytic subunit of DNA protein kinase (DNA-PKcs), which is recruited by DNA Ku protein, a heterodimer of Ku70 and Ku80, as well as XRCC4 protein and DNA ligase IV. A complex of Rad50/Mre11/Xrs2, a family of Sir proteins and probably other yet unidentified proteins can be also involved in this process. NHEJ and HR may play overlapping roles in the repair of DSBs produced in the S phase of the cell cycle or at replication forks. Aside from DNA repair, NHEJ may play a role in many different processes, including the maintenance of telomeres and integration of HIV-1 genome into a host genome, as well as the insertion of pseudogenes and repetitive sequences into the genome of mammalian cells. Inhibition of NHEJ can be exploited in cancer therapy in radio- sensitizing cancer cells. Identification of all key players and fundamental mechanisms underlying NHEJ still requires further research.

DNA-protection cross-linking induced by nitracrine in two strains of mouse lymphoma L5178Y cells

80%

Ciesielska E. , Walicka M. , Pastwa E. , Szmigiero L.

Acta Biochimica Polonica

1992

tom 39

nr 1

Inhibition of mammalian topoisomerase I by 1-nitro-9-aminoacridines. Dependence on thiol activation

80%

Ciesielska E. , Pastwa E. , Szmigiero L.

Acta Biochimica Polonica

1997

tom 44

nr 4

The cytotoxic activity, susceptibility to thiol activation and ability of eight 1-nitroacridine derivatives to stabilize the topoisomerase I-DNA cleavable complex, were compared. Among the acridines tested three compounds exhibited high ability to stabilize the cleavable complex. This ability was correlated with susceptibility to thiol activation as well as with cytotoxic activity. Our results suggest that 1-nitroacridine-DNA adducts interfering with topoisomerase I action may contribute to the lethal effects of some 1-nitroacridine derivatives.

DNA-protein crosslinks induced in HeLa cells by bis-1-nitroacridines

80%

Pastwa E. , Ciesielska E. , Studzian K. , Szmigiero L.

1993

tom 40

nr 1

Uptake of acridinecarboxamide derivatives by L1210 cells

61%

Ciesielska E. , Studzian K. , Bazylak G. , Pastwa E. , Denny W. A. , Szmigiero L.

Acta Biochimica Polonica

1998

tom 45

nr 4

The uptake of six 9-aminoacridinecarboxamide derivatives by L1210 cells in relation to their lipophilicity and cytotoxic activity was studied. The amount of acridines taken up by cells was estimated by fluorimetric measurements. It was found that the uptake efficiency of this class of compounds by cells depends on the size of carboxamide residue as well as on position of the substituent. The increase of size of carboxamide chain resulted in the loss of capability of acridines to penetrate cell membrane. Cytotoxic effects of acridines were well correlated with the level of drugs accumulated by cells, whereas no clear correlation between uptake and lipophilicity was observed. It is concluded that uptake of 9-aminoacridinecarboxamides is the most important factor determining their antiproliferative activity.