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1
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Telomery i telomeraza - starzenie komórkowe - nagroda Nobla z fizjologii lub medycyny 2009

100%
Sikora E.
Kosmos
|
2010
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vol. 59
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issue 1-2
1-8
EN
The 2009 Nobel Prize in Physiology or Medicine was awarded to Elizabeth H Blackburn, Jack W Szostak and Carol W Greider for their discovery of how chromosomes are protected by telomeres and the enzyme telomerase. They solved a fundamental problem in biology, namely how can the ends of chromosomes (telomeres) avoid erosion during cellular divisions. First, working on unicellular organisms, such as yeast and ciliate, they demonstrated that chromosomal ends have an evolutionary conserved structure and function. Then, in a series of meticulous biochemical studies, they revealed the existence of a previously predicted enzyme, named telomerase, responsible for the synthesis of telomeres. Telomerase appeared to be a nucleoprotein, reverse transcriptase with an intrinsic RNA template. The active telomerase was shown by others in cancer but not in normal somatic cells and telomere erosion was immediately considered as a "replicometer" or mitotic clock" counting divisions of somatic normal cells and inducing permanent cell growth arrest (replicative senescence). The discovery of telomerase has deeply influenced biomedical research and paved the way for the development of cancer therapies based on telomerase inhibition. However, subsequently it appeared that cellular senescence is beneficial because it protects the division of cells with short labile chromosomes being potentially prone to cancer transformation. Recently, it has been shown that senescence is a cell stress response to telomeric and nontelomeric DNA damage induced by oncogenic viruses, oxygen or genotoxic stress and critically short or nonfunctional telomeres, respectively. This reinforced the idea of cellular senescence as a cancer barrier but raised doubts in "replicometer" as a main cause of cellular senescence. However the story seems to be even more complicated and double-dealing as senescent cells secrete a myriad of factors, including pro-inflammatory cytokines, creating a microenvironment supporting organismal ageing and the development of age-related diseases, including cancer. Altogether, it seems, that the hopes put in telomerase as a key to eternal youth turned out to be vain.
2
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The impaired transcription factor AP-1 DNA binding activity in lymphocytes from subjects with some symptoms of premature aging

51%
Sikora E., Radziszewska E., Kmieć T., Maślińska D.
Acta Biochimica Polonica
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1993
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vol. 40
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issue 2
269-272
3
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Proliferation and apoptosis of human T cells during replicative senescence - a critical approach.

51%
Jaruga E., Skierski J., Radziszewska E., Sikora E.
Acta Biochimica Polonica
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2000
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vol. 47
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issue 2
293-300
EN
Normal human T lymphocytes growing in culture undergo replicative senescence. Previously, we have shown that in our conditions polyclonal T cells cease proliferation after about three weeks (Radziszewska et al., 1999, Cell Biol. Int. 23, 97-103). Now we present results of a more detailed analysis of in vitro growth as well as phenotypic changes of T cells. Cell cycle analysis showed that about 20% of cells were in the S phase untill the 17th day of culture (young cells). The highest number of mitotic cells (phase G2/M; 10%) was observed during the first week of culture. All not dividing senescent cells were stopped in the G1 phase (after the 30th day of culture). The sub-G1 fraction which represents apoptotic cells did not exceed 8% during the whole period until the 30th day of culture. During in vitro T-cell growth, a rather rapid selection to CD3+CD8+ cells occurs. In the presenescent (between the 17th and 30th day) and senescent populations the majority of cells (above 90%) were CD8 positive. We also have checked the expression of α-chain interleukin-2 (IL-2) receptor (CD25). In young and presenescent cells about one third of cells was CD25 positive, but only 15% in the pool of senescent cells. Immunoblotting analysis of p16 protein recognized previously as a marker of senescent T cells, showed its highest and transient expression in presenescent cells. A critical review of the polyclonal T cell replicative senescence model is presented.
4
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Effect of aging on UVC-induced apoptosis of rat splenocytes.

45%
Radziszewska E., Piwocka K., Bielak-Żmijewska A., Skierski J., Sikora E.
Acta Biochimica Polonica
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2000
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vol. 47
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issue 2
339-347
EN
UVC-induced apoptotic symptoms such as morphological changes, DNA fragmentation, Bcl-2 and Bax protein expression were examined in primary splenocyte cultures from young (3 months) and old (24 months) rats. The activities of AP-1 and CRE transcription factors in UVC-irradiated splenocytes were also assessed. At 24 h after UVC irradiation 40% of cells derived from young rats were found to be apoptotic, which was twice as much as in splenocytes from old rats. Apoptosis in cells from old rats did not give typical symptoms like a "DNA ladder" and Bcl-2 protein downregulation, in contrast to splenocytes from young rats. No AP-1 transcription factor activity was found in UVC-irradiated splenocytes from old animals and only a trace activity in splenocytes from young animals. This indicates that, UVC-induced apoptosis in rat splenocytes is practically AP-1 independent and that cells from old rats are less sensitive to UVC irradiation than splenocytes from young rats.
5
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A quinazoline antifolate as inhibitor of folate metabolism in mouse L-cells

45%
Sikora E., Grzelakowska-Sztabert B.
Acta Biochimica Polonica
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1983
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vol. 30
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issue 2
193-201
6
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Interference between DNA binding activities of AP-l and GR transcription factors in rat thymocytes undergoing dexamethasone-induced apoptosis

39%
Sikora E., Rossini G. P., Grassilli E., Bellesia E., Salomoni P., Franceschi C.
Acta Biochimica Polonica
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1996
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vol. 43
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issue 4
721-731
7
Content available remote

Curcumin induces cell death without oligonucleosomal DNA fragmentation in quiescent and proliferating human CD8+ cells

39%
Magalska A., Brzezinska A., Bielak-Zmijewska A., Piwocka K., Mosieniak G., Sikora E.
Acta Biochimica Polonica
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2006
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vol. 53
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issue 3
531-538
EN
Cytotoxic CD8+ cells play an important role in determining host response to tumor, thus chemotherapy is potentially dangerous as it may lead to T cells depletion. The purpose of this study was to elucidate the propensity of quiescent and proliferating human CD8+ cells to undergo cell death upon treatment with curcumin, a natural dye in Phase I of clinical trials as a prospective chemopreventive agent. Methods: We treated human quiescent or proliferating CD8+ cells with 50 µM curcumin or irradiated them with UVC. Cell death symptoms such as decreased cell viability, chromatin condensation, activation of caspase-3 and specific DFF40/CAD endonuclease and oligonucleosomal DNA fragmentation were analyzed using MTT test, microscopic observation, Western blotting and flow cytometry. Results: Curcumin decreased cell viability, activated caspase-3 and decreased the level of DFF45/ICAD, the inhibitor of the DFF40/CAD endonuclease. However, this did not lead to oligonucleosomal DNA degradation. In contrast, UVC-irradiated proliferating, but not quiescent CD8+ cells revealed molecular and morphological changes characteristic for apoptosis, including oligonucleosomal DNA fragmentation. Curcumin can induce cell death in normal human lymphocytes both quiescent and proliferating, without oligonucleosomal DNA degradation which is considered as a main hallmark of apoptotic cell death. Taking into account the role of CD8+ cells in tumor response, their depletion during chemotherapy could be particularly undesirable.
8
Content available remote

Transcription factors in cellular senescence and death

32%
Sikora E.
Acta Biochimica Polonica
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1993
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vol. 40
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issue 3
389-394
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