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1

Cytogenetic assay in apoptosis investigations

100%
Akopyan H., Sirenko A., Sedneva I., Jakimovich M., Stojka R., Hnatejko O.
Folia Histochemica et Cytobiologica. Supplement
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2001
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tom 39
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nr 1
2

Study on the activity of the signaling pathways regulating hepatocytes from G0 phase into G1 phase during rat liver regeneration

75%
Li M., Zhou X., Mei J., Geng X., Zhou Y., Zhang W., Xu C.
Cellular and Molecular Biology Letters
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2014
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tom 19
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nr 2
Under normal physiological conditions, the majority of hepatocytes are in the functional state (G0 phase). After injury or liver partial hepatectomy (PH), hepatocytes are rapidly activated to divide. To understand the mechanism underlying hepatocyte G0/G1 transition during rat liver regeneration, we used the Rat Genome 230 2.0 Array to determine the expression changes of genes, then searched the GO and NCBI databases for genes associated with the G0/G1 transition, and QIAGEN and KEGG databases for the G0/G1 transition signaling pathways. We used expression profile function (E t ) to calculate the activity level of the known G0/G1 transition signal pathways, and Ingenuity Pathway Analysis 9.0 (IPA) to determine the interactions among these signaling pathways. The results of our study show that the activity of the signaling pathways of HGF, IL-10 mediated by p38MAPK, IL-6 mediated by STAT3, and JAK/STAT mediated by Ras/ERK and STAT3 are significantly increased during the priming phase (2–6 h after PH) of rat liver regeneration. This leads us to conclude that during rat liver regeneration, the HGF, IL-10, IL-6 and JAK/STAT signaling pathways play a major role in promoting hepatocyte G0/G1 transition in the regenerating liver.
3
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Sucrose uptake and transport are inhibited by okadaic acid during regeneration of the sugar-starved Vicia faba root meristem cells

51%
Polit J. T., Zabka A.
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
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2013
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tom 94
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nr 3
4

RNAi mediated silencing of cyclin-dependent kinases of G1 phase slows down the cell-cycle progression and reduces apoptosis

51%
Sierant M., Piotrzkowska D., Nawrot B.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr 1
One of the hypotheses on the origin of Alzheimer's disease (AD) stems from a close relation between a re-activation of a cell-cycle in post-mitotic neurons and a neural cells death observed in pathologically affected parts of AD brains. In the normal, healthy brain almost all neural cells are terminally differentiated and "locked" in the GO phase of the cell-cycle. For these cells, the consequence of the re-entry to the cell-cycle is targeting them towards cellular divisions and turning on the apoptotic pathway. We used an RNA interference (RNAi) methodology in neural cells to switch-off genes for two cyclin- dependent kinases 4 and 6 (cdk4, cdk6), which control the activation of the initial steps of the cell-cycle. As a result, some evidences are delivered that silencing these genes, which are expressed during cell proliferation but inhibited at mature neurons, prevents the stimulation of apoptotic pathways in the neural cells cultured in a oxidative stress conditions and may have a neuroprotective effect. We demonstrate that down-regulation of genes important in the G1 phase of the cell-cycle may play the protective function on the neuronal cells, and can be considered as the promising approach for the potential gene therapy of neurodegenerative diseases.
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Alterations in TP53, cyclin D2, c-Myc, p21WAF1/CIP1 and p27KIP1 expression associated with progression in B-CLL

51%
Antosz H., Paterski A., Marzec-Kotarska B., Sajewicz J., Dmoszynska A.
Folia Histochemica et Cytobiologica
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2010
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tom 48
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nr 4
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