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Erfahrungen mit UTH 1424 bei der Bekampfung von Musca domestica

100%

Muller P.

Wiadomości Parazytologiczne

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1982

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tom 28

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nr 1-2

2

Continuous record of the evolution of lacustrine cardiid bivalves in the late Miocene Pannonian Lake

63%

Muller P., Magyar I.

Acta Palaeontologica Polonica

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1991

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tom 36

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nr 4

A biometric study was performed on populations of lacustrine cardiid bivalves in stratigraphically ordered samples from the deposits of a late Miocene lake, which are exposed close to Lake Balaton in Hungary. The lineage can be subdivided into several chronospecies: it starts from Lymnocardium decorum ponticum and leads to the genus Prosodacnomya which is considered to belong to another subfamily than Lymnocardium. The evolutionary process was gradual, microevolutionary, anagenetic, and possibly peramorphic. Certain populations displayed ecophenotypic changes that were similar in their nature to the observed evolutionary ones. The shells exhibit a gradual fusion of the central ribs, resulting in a smooth central zone in late populations. The process could be an adaptation to conditions present in shallow regions of an endorheic lake with frequently displaced shoreline where ploughing was more important than digging. The smooth central zone leads to decreased friction during ploughing. The estimated time span of the evolution is between one and three million years.

3

Alterations of the Hsp70/Hsp90 chaperone and the HOP/CHIP co-chaperone system in cancer

51%

Ruckova E., Muller P., Nenutil R., Vojtesek B.

Cellular and Molecular Biology Letters

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2012

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tom 17

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nr 3

Activation of the Hsp90 chaperone system is a characteristic of cancer cells. The regulation of chaperone activities involves their interaction with cochaperones; therefore we investigated the expression of Hsp70 and Hsp90 and their specific co-chaperones HOP and CHIP in cancer cell lines and primary cancers. Inhibition of Hsp90 by 17AAG increased the levels of Hsp70, Hsp90 and HOP but not CHIP mRNA in cancer cells. These changes are linked to activation of the HSF1 transcription factor and we show that the HOP promoter contains HSF1 binding sites, and that HSF1 binding to the HOP promoter is increased following 17AAG. The lack of alteration in the co-chaperone CHIP is explained by a lack of HSF response elements in the CHIP promoter. Non-proliferating cells expressed higher levels of CHIP and lower HOP, Hsp70 and Hsp90 levels compared to proliferating cells. Decreased expression of CHIP in proliferating cancer cells is in keeping with its proposed tumor suppressor properties, while over-expression of HOP in proliferating cells may contribute to excessive Hsp90 activity and stabilization of client proteins in tumors. In a panel of colorectal cancer samples, increased expression of Hsp70 and an increased ratio of HOP to CHIP were found, and were associated with decreased median survival. These data indicate that multiple changes occur in the chaperone/co-chaperone system in cancer that impact patient survival. It is likely that the ability to identify individual alterations to this system will be beneficial for treatment strategy decisions, particularly those that employ chaperone inhibitors.

4

Compression and flow behaviour of cohesive powders

51%

Stasiak M., Tomas J., Molenda M., Muller P.

Electronic Journal of Polish Agricultural Universities. Series Agricultural Engineering

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2009

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tom 12

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nr 2

5

A new glimpse on trophic interactions of 100-million-year old lacewing larvae

45%

Hornig M. K., Kiesmuller C., Muller P., Haug C., Haug J. T.

Acta Palaeontologica Polonica

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2020

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tom 65

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nr 4

6

Cyclin-dependent kinase inhibitor olomoucine II interacts with CDK2 and CDK9

39%

Krystof V., Orsag M., Paprskarova M., Muller P., Vojtesek B., Strnad M.

Cellular and Molecular Biology Letters

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2005

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tom 10

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nr Suppl.2

7

The cell type-specific effect of TAp73 isoforms on the cell cycle and apoptosis

33%

Holcakova J., Ceskova P., Hrstka R., Muller P., Dubska L., Coates P. J., Palecek E., Vojtesek B.

Cellular and Molecular Biology Letters

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2008

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tom 13

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nr 3

404-420

p73, a member of the p53 family, exhibits activities similar to those of p53, including the ability to induce growth arrest and apoptosis. p73 influences chemotherapeutic responses in human cancer patients, in association with p53. Alternative splicing of the TP73 gene produces many p73 C- and N-terminal isoforms, which vary in their transcriptional activity towards p53-responsive promoters. In this paper, we show that the C-terminal spliced isoforms of the p73 protein differ in their DNA-binding capacity, but this is not an accurate predictor of transcriptional activity. In different p53-null cell lines, p73β induces either mitochondrial-associated or death receptor-mediated apoptosis, and these differences are reflected in different gene expression profiles. In addition, p73 induces cell cycle arrest and p21WAF1 expression in H1299 cells, but not in Saos-2. This data shows that TAp73 isoforms act differently depending on the tumour cell background, and have important implications for p73-mediated therapeutic responses in individual human cancer patients.

Ograniczanie wyników

Erfahrungen mit UTH 1424 bei der Bekampfung von Musca domestica

Continuous record of the evolution of lacustrine cardiid bivalves in the late Miocene Pannonian Lake

Alterations of the Hsp70/Hsp90 chaperone and the HOP/CHIP co-chaperone system in cancer

Compression and flow behaviour of cohesive powders

A new glimpse on trophic interactions of 100-million-year old lacewing larvae

Cyclin-dependent kinase inhibitor olomoucine II interacts with CDK2 and CDK9

The cell type-specific effect of TAp73 isoforms on the cell cycle and apoptosis