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1

Regulation of calcium signals in animal cell-role of mitochondria

100%
Zablocki K.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
2

Żródła bezrobocia na wsi

100%
Zablocki K.
Wieś i Rolnictwo
|
1997
|
nr 3
3

Osmolity i osmoregulacja w komorkach nerek

63%
Wieckowsi M., Zablocki K.
Postępy Biochemii
|
1996
|
tom 42
|
nr 2
167-177
4

Mitochondria w życiu, chorobie i śmierci komórki

63%
Wojtczak L., Zablocki K.
Postępy Biochemii
|
2008
|
tom 54
|
nr 2
5

Mitochondria in intracellular signalling pathways

63%
Zablocki K.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr Supplement 4
6

Effect of ciprofloxacin on mitochondrial energy metabolism, calcium signaling and viability of Jurkat T-cells

51%
Koziel R., Zablocki K., Duszynski J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
7

Choroby spowodowane mutacjami w mitochondrialnym DNA

51%
Wojewoda M., Zablocki K., Szczepanowska J.
Postępy Biochemii
|
2011
|
tom 57
|
nr 2
8

Mitochondrial uncoupling does not influence the stability of the intracellular signal activating plasma membrane calcium channels

51%
Zablocki K., Makowska A., Duszynski J.
Acta Biochimica Polonica
|
2001
|
tom 48
|
nr 1
The effects of various concentrations of thapsigargin, a specific inhibitor of Ca2+ -ATPase in the endoplasmic reticulum (ER) membrane, on calcium homeostasis in lymphoidal T cells (Jurkat) were investigated. Preincubation of these cells suspended in nominally calcium-free medium with 0.1 UM thapsigargin resulted in a complete release of Ca2+ from intracellular calcium stores. When the medium was supplemented with 3 mM CaCl2 the cells maintained constantly elevated level of cytosolic Ca2+ . However, tha­psigargin applied at lower concentration produced only a partial depletion of the stores. For example, in the cells pretreated with 1 nM thapsigargin and suspended in calcium-free medium approximately 75% of the calcium content was released from the intracellular stores. The addition of 3 mM CaCl2 to such cell suspension led to a transient increase in cytosolic calcium concentration, followed by a return to a lower steady-state. This phenomenon, related to the refilling of the ER by Ca2+ , allowed to estimate the half-time for the process of cell recovery after activation of store-operated calcium channels. By this ap­proach we have found that carbonyl cyanide m-chlorophenylhydrazone, which has been documented to inhibit calcium entry into Jurkat cells, does not influence the stability of the intracellular signal involved in the activation of store-operated calcium channels.
9

Participation of phospholipase A2 isoforms in the control of calcium influx into electrically non-excitable cells

51%
Zablocki K., Wasniewska M., Duszynski J.
Acta Biochimica Polonica
|
2000
|
tom 47
|
nr 3
The participation of phospholipase A2 isoforms in capacitative store-operated Ca2+ influx into Jurkat leukemic T and MDCK cells was investigated. Preincubation of Jurkat cells with either bromophenacyl bromide (an inhibitor of secreted phospholipase A2, sPLA2) or Helss (an inhibitor of calcium independent phospholipase A2 iPLA2) resulted in a significant inhibition of the calcium influx. The extent of this inhibition depended on the pH of the extracellular millieu; it increased with alkalisation. The rate of Ca2+ influx into MDCK cells was reduced by bromophenacyl bromide. Preincubation of these cells with Helss resulted in the stimulation of the influx. These observations suggest the participation of different PLA2 isoforms in the regulation of Ca2+ influx. They also show that the extent that PLA2 isoforms control the influx depends on the pH of the medium. Finally, these data indicate that various phospholipase A2 isoforms may play a role in the control of Ca2+ influx in different cell lines.
10

The pH-dependent effect of mitochondria on Ca2plus influx into Jurkat cells

51%
Zablocki K., Makowska A., Szczepanowska J., Duszynski J.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr Suppl.
11

AS-30D hepatoma as a model to study on insulin resistance in vitro

45%
Wierzbicka-Bregier K., Brutkowski W., Borkowska A., Milewski K., Zablocki K.
Acta Biochimica Polonica
|
2013
|
tom 60
|
nr 4
Studies on insulin resistance of liver cells are often performed with the use of various hepatoma cell lines. Such an approach allows investigating selected biochemical pathways at the cellular level. However, possible modifications of metabolic processes due to the neoplastic nature of such cells must be considered. Expanding the diversity of hepatoma cell lines used in metabolic studies could deliver new data for comparison with those obtained for other cell lines and should reduce the risk of misleading conclusions. In this study rat hepatoma AS-30D cells were tested as a potential model for studies on palmitate-induced insulin resistance. It was found that insulin-induced Akt kinase phosphorylation was substantially reduced in cells incubated with palmitate at a concentration as low as 75 µM. This effect was not accompanied by excessive reactive oxygen species (ROS) generation or increased Jun N-terminal kinase (JNK) phosphorylation. Moreover, preincubation of AS-30D cells with rosiglitazone, an antidiabetic agonist of peroxisome proliferator-activated receptor gamma (PPARγ), efficiently prevented the palmitate-induced insulin resistance. We conclude that AS-30D hepatoma cells may be used as a model sensitive to insulin and vulnerable to palmitate-induced insulin resistance.
12

Role of calcium-independent phospholipase A2 in the UV-induced apoptosis in Jurkat cells

45%
Zablocki K., Bielak A., Piwocka K., Wojtczak L., Duszynski J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
13
Content available remote

Ciprofloxacin inhibits proliferation and promotes generation of aneuploidy in Jurkat cells

39%
Koziel R., Szczepanowska J., Magalska A., Piwocka K., Duszynski J., Zablocki K.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 2
Ciprofloxacin is widely used in antimicrobial therapy. However it also inhibits mitochondrial topoisomerase II and therefore affects cellular energy metabolism. At a concentration exceeding 80 µg/ml ciprofloxacin induces apoptosis, while at 25 µg/ml it inhibits proliferation of Jurkat cells without any symptoms of cell death. The aim of this study was to explain the mechanisms of ciprofloxacin-evoked perturbations of the cell cycle. Human lymphoidal cells (Jurkat) were exposed to ciprofloxacin (25 µg/ml) for 4-11 days and effects of the drug on cell proliferation (light microscopy), cell cycle (flow cytometry), cell size and morphology (confocal microscopy) as well as number of chromosomes (chromosomal spread analysis) were investigated. Exposition of Jurkat cells to ciprofloxacin inhibited cell proliferation, increased proportion of cells in the G2/M-phase of the cell cycle, compromised formation of the mitotic spindle and induced aneuploidy. These observations indicate that ciprofloxacin applied at concentrations insufficient for induction of apoptosis may stop cell proliferation by inhibition of mitosis. Chromosomal instability of such cells may, at least potentially, increase a risk of cancer development.
14
Content available remote

Large-conductance K+ channel openers induce death of human glioma cells

33%
Debska-Vielhaber G., Godlewski M. M., Kicinska A., Skalska J., Kulawiak B., Piwonska M., Zablocki K., Kunz W. S., Szewczyk A., Motyl T.
Journal of Physiology and Pharmacology
|
2009
|
tom 60
|
nr 4
27-36
Large-conductance Ca2+-activated K+ channels (BKCa channels) are highly expressed in human glioma cells. It has been reported that BKCa channels are present in the inner mitochondrial membrane of the human glioma cell line LN229. In the present study we investigated whether BKCa-channel openers, such as CGS7181 (ethyl 2-hydroxy-1-[[(4-methylphenyl)amino]oxo]-6-trifluoromethyl-1H-indole-3-carboxylate) and CGS7184 (ethyl 1-[[(4-chlorophenyl) amino]oxo]-2-hydroxy-6-trifluoromethyl-1H-indole-3-carboxylate), affect the functioning of LN229 glioma cell mitochondria in situ. In the micromolar concentration range CGS7181 and CGS7184 induced glioma cell death. Morphological and cytometric analyses confirmed that both substances trigger the glioma cell death. This effect was not inhibited by the pan-caspase inhibitor z-VAD-fmk. Lack of DNA laddering, PARP cleavage, and caspase 3 activation suggested that glioma cell death was not of the apoptotic type. We examined the effect of CGS7184 on mitochondrial membrane potential and mitochondrial respiration. Potassium channel opener CGS7184 increased cell respiration and induced mitochondrial membrane depolarization. The latter was dependent on the presence of Ca2+ in the external medium. It was shown that CGS7184 induced an increase of cytosolic Ca2+ concentration due to endoplasmic reticulum store depletion. In conclusion, our results show that CGS7181 and CGS7184 induce glioma cell death by increasing the cytosolic calcium concentration followed by activation of calpains.
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