Wyniki wyszukiwania

1

Adenosine 5'-triphosphate - a new regulator of annexin function. A hypothesis

100%

Bandorowicz-Pikula J., Pikula S.

Acta Biochimica Polonica

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1998

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tom 45

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nr 3

The paradigm of annexins as phospholipid-binding proteins interacting with membranes in a calcium-dependent manner has been recently questioned in light of observations that some annexin isoforms may behave like membrane integral proteins or remain associated with their target membranes at low, resting, concentrations of Ca2+ in the cytoplasm. In addition, an evidence has been presented that some annexins (annexins I, VI and VII) bind in vitro ATP and GTP, and upon binding the nucleotide the in vitro activity of these proteins is modified. However, annexins do not contain Walker A and B consensus sequences for ATP/GTP binding. This review presents the hypothesis that a new ATP-binding motif exists within the annexin molecules and that ATP may play a role of functional ligand for annexins also in vivo

2

Amphibian calcium regulation: physiological aspects

100%

Srivastav A. K., Das V. K., Srivastav S. K., Suzuki N.

Zoologica Poloniae

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2000

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tom 45

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nr 1-4

3

Differential expression of genes involved in the calcium homeostasis in masticatory muscles of mdx mice

84%

Kunert-Keil C., Gredes T., Lucke S., Brotzenhart U., Dominiak M., Gedrange T.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 2

4

Plasma membrane Ca2plus -ATPase in excitable and nonexcitable cells

84%

Zylinska L., Soszynski M.

Acta Biochimica Polonica

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2000

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tom 47

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nr 3

There is a significant number of data confirming that the maintenance of calcium homeostasis in a living cell is a complex, multiregulated process. Calcium efflux from excitable cells (i.e., neurons) occurs through two main systems an electrochemically driven Na+/Ca2+ exchanger with a low Ca2+ affinity (K0.5 = 10-15 µM), and a plasmalemmal, specific Ca2+-ATPase, with a high Ca2+ affinity (K0.5 <0.5-1 µM), whereas in nonexcitable cells (i.e., erythrocytes) the calcium pump is the sole system responsible for the extrusion of calcium ions. The plasma membrane Ca2+-ATPase (PMCA) is a ubiquitously expressed protein, and more than 26 transcripts of four PMCA genes are distributed in a tissue specific manner. Differences in the structure and localization of PMCA variants are thought to correlate with specific regulatory properties and may have consequences for proper cellular Ca2+ signaling. The regulatory mechanisms of calcium pump activity have been studied extensively, resulting in a new view of the functioning of this important molecule in the membranes.

5

Influence of vitamin D3 analogues in combination with budesonid R on proliferation of nasal polyp fibroblasts

67%

Rostkowska-Nadolska B., Fraczek M., Gawron W., Latocha M.

Acta Biochimica Polonica

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2009

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tom 56

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nr 2

235-242

Vitamin D (VD) and its different analogues, besides their classic role as regulators of calcium and phosphor homeostasis, have emerged as a large family of antiproliferative agents. Such properties suggested VD potential as a therapy for chronic inflammatory diseases, including nasal polyposis (NP). NP growth involves both an inflammatory process and the proliferation of fibroblast as an important factor inducing aberrations in the phenotype of the epithelium. The aim of this study was to investigate the possible influence of 1α,25-dihydroxyvitamin D3 (calcitriol) and 1α,24(R)-dihydroxyvitamin D3 (tacalcitol) in monotherapy and in combination with budesonid R (BR) on NP fibroblast proliferation. Material and methods: The study involved 26 samples of NP. NP cells were cultured on 96-well plates beginning with a concentration of 5 × 103 cells per well with RPMI 1640 medium supplemented with antibiotics and 10% foetal bovine serum. After the fourth to sixth passage the medium was replaced with a nutrient medium with calcitriol or tacalcitol in a defined concentration (from 10-9 M to 10-3 M) alone or in combination with BR in 1:1, 1:3 or 3:1 ratios, each at concentrations from 10-5 M to 10-3 M. Results: Growth inhibition of nasal fibroblasts exposed to calcitriol or tacalcitol was noted. Significant antiproliferating activity was observed at calcitriol concentrations of 10-4 M and 10-3 M after 48 h, and at a concentration of 10-3 M after 72 h with the percentage of proliferating cells reduced to 30% compared to the control samples (P < 0.05). In cells treated with tacalcitol the maximal effect was seen at 10-4 M after 48 h and at 10-3 M after 72 h with a 60% inhibition with respect to the control (P < 0.05). The inhibition of fibroblast proliferation reached the maximal level when they were exposed to calcitriol: BR (1 : 1) or tacalcitol: BR (1 : 1), each at a concentration of 10-4 M, after 72 h (82% and 69%, respectively). Conclusions: The antiproliferative activity of calcitriol and tacalcitol in NP cultures was confirmed. Because of its lower toxicity and higher activity tacalcitol seems to be the more promising agent in NP therapy, both as a single medication and in treatment protocols with BR.

6

Mitochondrial integrity and function in model systems of CNS diseases

67%

Culmsee C.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

Mitochondria are key regulators of energy metabolism, redox balance, calcium homeostasis, and programmed cell death. In the past, we characterized mitochondria acting as targets of both caspase-dependent and caspase- independent death signalling triggered by increased oxidative stress and as executioners of programmed death signalling in neurons. For example, we identified mitochondrial damage in caspase‑independent neuronal death after cerebral ischemia in vivo, and in oxidative cell death, i.e., ferroptosis in vitro. Protective intervention against oxidative damage further confirmed the conclusion that mitochondria represent the “point of no return” in caspase‑independent paradigms of programmed cell death. Further, we found more recently that mitochondri al-targeted alpha-synuclein caused severe mitochondrial toxicity and caspase-dependent cell death in human dopaminergic neurons, a model system relevant to Parkinson’s disease. In different model systems of neuronal death, neuroprotective interference with mitochondrial pathways of programmed cell death was frequently attributed to metabolic switches, i.e., reduced mitochondrial respiration and increased glycolytic activity. Accordingly, targeting metabolic switches may serve as a general strategy for mitochondrial protection and, thereby, neuroprotection, but may also affect mechanisms of neuroinflammation involving activation of microglia. The understanding of the underlying mechanism of such metabolic protection may reveal novel therapeutic targets in neural diseases featuring mitochondrial impairments and neuroinflammation.

7

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Gamma-secretase complex in plant cells

67%

Skrzypczak T., Smolarkiewicz M., Wojtaszek P.

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

8

The structure of the Ca2plus -ATPase of sarcoplasmic reticulum

67%

Martonosi A. N., Pikula S.

Acta Biochimica Polonica

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2003

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tom 50

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nr 2

In this article the morphology of sarcoplasmic reticulum, classification of Ca2+ -ATPase (SERCA) isoenzymes presented in this membrane system, as well as their topology will be reviewed. The focus is on the structure and interactions of Ca2+ -ATPase determined by electron and X-ray crystallog2r+aphy, lamellar X-ray and neutron diffraction analysis of the profile structure of Ca2+ -ATPase in sarcoplasmic reticulum multilayers. In addition, targeting of the Ca2+ -ATPase to the sarcoplasmic reticulum is discussed.

9

Side-chain modified vitamin D analogs require activation of both PI 3-K and erk1,2 signal transduction pathways to induce differentiation of human promyelocytic leukemia cells

67%

Marcinkowska E., Kutner A.

Acta Biochimica Polonica

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2002

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tom 49

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nr 2

Synthetic analogs of vitamin D for potential use in differentiation therapy should selectively regulate genes necessary for differentiation without inducing any perturbations in calcium homeostasis. PRI-1906, an analog of vitamin D2, and PRI-2191, an analog of vitamin D3 bind nuclear vitamin D receptor (nVDR) with substantially lower affinity than 1,25-dihydroxyvitamin D3 (1,25-D3), but have higher differentiation-inducing activity as estimated in HL-60 leukemia cell model. To examine how their increased differentiation-inducing activity is regulated we tested the hypothesis that membrane-mediated events, unrelated to nVDR, take part in the differentiation in response to PRI-1906 and PRI-2191. The induction of leukemia cell differentiation in response to the analogs of vitamin D was inhibited by LY294002 (phosphatidyl- inositol 3-kinase inhibitor), PD98059 (inhibitor of MEK1,2, an upstream regulator of extracellular-signal regulated kinase) and rapamycin (p70 S6K inhibitor) pointing out that activation of signal transduction pathways unrelated to nVDR is necessary for differentiation. On the other hand, inhibition of cytosolic phospholipase A2 accelerated the differentiation of HL-60 cells induced by either 1,25-D3 or by the vitamin D analogs suggesting possible existence of a feedback loop between extracellular-signal regulated kinases and phospholipase A2.

Ograniczanie wyników

Adenosine 5'-triphosphate - a new regulator of annexin function. A hypothesis

Amphibian calcium regulation: physiological aspects

Differential expression of genes involved in the calcium homeostasis in masticatory muscles of mdx mice

Plasma membrane Ca2plus -ATPase in excitable and nonexcitable cells

Influence of vitamin D3 analogues in combination with budesonid R on proliferation of nasal polyp fibroblasts

Mitochondrial integrity and function in model systems of CNS diseases

Gamma-secretase complex in plant cells

The structure of the Ca2plus -ATPase of sarcoplasmic reticulum

Side-chain modified vitamin D analogs require activation of both PI 3-K and erk1,2 signal transduction pathways to induce differentiation of human promyelocytic leukemia cells