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Modulation of buccal mucosal calcium channel activity by salivary mucins

100%

Slomiany B. L., Fekete Z., Murty L. N., Slomiany A.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 3

2

Regulation of exocytosis by cytoskeleton in neuroendocrine cells

100%

Gasman S., Chasserot-Golaz S., Bader M. F., Aunis D.

Cellular and Molecular Biology Letters

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1998

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tom 03

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nr 2

3

Regulation of non-clathrin endocytosis

100%

Kotula L.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

4

cAMP-dependent protein kinase: structural basis for function, regulation, and subcellular localization

100%

Taylor S. S., Narayana N., Huang L., Banky P., Wang L., Cheng X.

Cellular and Molecular Biology Letters

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1998

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tom 03

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nr 3

5

Regulation of synaptic functions by modification of postsynaptic density proteins

88%

Sheng M.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Phosphorylation regulation of postsynaptic density proteins is likely to be a major means of regulating synaptic function. The PSD scaffold PSD-95, a powerful determinant of synaptic strength, is a case in point. Its precise role during synaptic plasticity (LTP versus LTD) has not been easy to interpret from overexpression, RNAi or knockout mice experiments. We found that the PSD scaffold PSD-95 is phosphorylated on multiple sites in cultured neurons and in vivo. Ser-295 phosphorylation, mediated by a Rac1-JNK1 MAP kinase pathway and countered by phosphatases PP1 or PP2A, promotes PSD-95 accumulation in synapses and is associated with LTP-inducing stimuli. More strikingly, LTD-inducing stimuli causes dephosphorylation of ser-295 rapidly and profoundly, correlating with activation of PP1. In addition, LTD was associated with phosphorylation of an N-terminal residue of PSD-95 by the protein kinase GSK3b. This site is also bidirectionally modulated by activity. A phospho-mimicking mutant of PSD-95 (S295DPSD-95; which cannot be “dephosphorylated”) impaired the internalization of AMPA receptors in cultured neurons and blocked the induction of LTD in cultured hippocampal slices. Our data indicate that dephosphorylation of PSD-95 on ser295, and phosphorylation of the N-terminus of PSD-95, is required for mobilization of PSD-95 from the PSD, de-anchoring of AMPA receptors from the PSD for internalization, and hence induction of LTD.

6

The role of membrane fluidity in regulation of molecular mechanism of the xanthophyll cycle

88%

Strzalka K., Latowski D., Burda K.

Polish Journal of Natural Sciences. Supplement

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2003

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tom 01

7

Neurohormonal mechanisms of regulation of insect heart contractile activity

88%

Rosinski G., Konopinska D.

Pestycydy

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2004

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nr 3-4

8

Regulation of gastric mucosal calcium channel activity by an antiulcer agent, ebrotidine

88%

Slomiany B. L., Liu J., Piotrowski J., Czajkowski A., Yotsumoto F., Slomiany A.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 1

9

A statistical procedure [CHAIN] to study protein kinase structural mechanisms

88%

Kannan N., Af N.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 2A

10

Role of rpoS in the regulation of glyoxalase III in Escherichia coli

88%

Benov L., Sequeira F., Beema A. F.

Acta Biochimica Polonica

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2004

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tom 51

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nr 3

Methylglyoxal is an endogenous electrophile produced in Escherichia coli by the enzyme methylglyoxal synthase to limit the accumulation of phosphorylated sugars. In enteric bacteria methylglyoxal is detoxified by the glutathione-dependent glyoxalase I/II system, by glyoxalase III, and by aldehyde reductase and alcohol dehydrogenase. Here we demonstrate that glyoxalase III is a stationary-phase enzyme. Its activity reached a maximum at the entry into the stationary phase and remained high for at least 20 h. An rpoS- mutant displayed normal glyoxalase I and II activities but was unable to induce glyoxalase III in stationary phase. It thus appears that glyoxalase III is regulated by rpoS and might be important for survival of non-growing E. coli cultures.

11

Deregulation of the profession of an urban planner in Poland in terms of Polish and community regulations

75%

Koltys R.

Człowiek i Środowisko

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2014

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tom 38

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nr 2

12

Legal and social aspects of biotechnology development

75%

Twardowski T.

Acta Biologica Cracoviensia. Series Botanica. Supplement

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2005

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tom 47

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nr 1

13

Epigenetic mechanisms of gene expression regulation in neurological diseases

75%

Gos M., Rzonca S., Szopa D., Abramowicz A., Bal J.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Neurological diseases, including intellectual disability (ID), can be caused by disturbances in epigenetic regulation of specific genes that encode proteins necessary for appropriate central nervous system functioning. The “epigenetically caused” diseases can be due to the imprinting defects formed during germinal cells development or gained throughout life as a somatic changes. They can also result from abnormal functioning of transcriptional machinery caused by mutations in genes coding for specific proteins. Two most classical examples of disease caused by imprinting defect in germinal cells are Prader-Willi and Angelman syndromes, both characterized by ID and developmental delay. Both these diseases are caused by altered epigenetic regulation of genes localized on chromosome 15 (region q11–q13) that can be due to chromosome deletion or uniparental disomy. The other neurological disease that is related to abnormal epigenetic regulation is Fragile X syndrome characterized by ID and specific behavior. Almost all disease cases are due to the expansion of CGG repeat (>200) in the 5’UTR of FMR1 gene that leads to promoter methylation and lack of FMRP protein that is indispensable for neuron development and signaling. The example of neurological “epigenetic diseases” caused by altered transcriptional regulation is Rett syndrome caused by the mutation presence in MECP2 gene or its variant – Rett-like syndrome caused by the mutation in CDKL5 gene. Both these diseases are characterized by ID and childhood epilepsy. Herein, we present our experience from the research and diagnosis of above mentioned disorders in the context of neurological pathways altered by improper epigenetic regulation.

14

Changes in the compensation system of management boards of German companies after the financial and economic crisis

75%

Stawarczyk F. M.

Folia Pomeranae Universitatis Technologiae Stetinensis. Oeconomica

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2012

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tom 69

15

Central and local (enteric) action of orexins

75%

Korczynski W., Ceregrzyn M., Matyjek R., Kato I., Kuwahara A., Wolinski J., Zabielski R.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 6

17-42

Orexin-A (OXA, hyprocretin-1) and orexin-B (OXB, hypocretin-2) are peptides derived from the same 130 amino acid long precursor (prepro-orexin) that bind and activate two closely related orphan G protein-coupled receptors. Orexins and their receptors were first discovered in the rat brain, and soon after that in peripheral neural structures, including the vagal nerve and enteric nervous system, and in other structures involving the gastrointestinal tract diffuse neuroendocrine system, pancreas tissue, stomach and intestinal mucosa. Orexins and their receptors were also demonstrated in the testes, adrenals, kidneys and placenta. This review is focused on central and enteric actions. Originally, orexins were considered to be neurotransmitters that centrally stimulate food intake in animals and humans, but it soon became evident that their action is broader due to activation of a large number of neuronal pathways involved in energy homeostasis, sleep-awake behavior, nociception, reward seeking, food and drug addiction, as well as reproduction, cardiovascular and adrenal function. In the gastrointestinal tract, orexins have been found so far to affect gastrointestinal motility and gastric, intestinal and pancreatic secretions. The effects were observed following central (intraventricular) or local (intraluminal, intraarterial), but not peripheral (intravenous), administrations of orexins. Since the expression of orexins in the gastrointestinal tract is enhanced during fasting, and fasting reveals many of the orexin gastrointestinal effects, it seems probable that on the local level, orexins keep the gastrointestinal tract functions ready during fasting and play a role in brain-gut axis control.

16

The isoform- and location-dependence of the functioning of the plasma membrane calcium pump

75%

Zylinska L., Kawecka I., Lachowicz L., Szemraj J.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr 4

The plasma membrane is a specialised multi-component structure with inter- and intracellular signalling functions. Ca2+ plays a crucial role in cellular physiology, and an ATP-driven plasma membrane calcium pump (PMCA) plays the greatest role in the maintenance of a low free Ca2+ concentration in the cytoplasm. The enzyme is coded by four separate genes (PMCA 1-4), and, due to alternative splicing, more than 20 variants can exist. PMCA 1 and 4 isoforms are present in almost all tissues, whereas PMCA 2 and 3 are found in more specialised cell types. The variants differ primarily in their regulatory regions, thus the modulation of calcium pump activity strongly depends on the isoform and the membrane composition. The unique function of PMCA isoforms was confirmed using the practical experimental models - a rat pheochromocytoma cell line, a human neuroblastoma cell line, or, more recently, knockout mice. In addition, based on the finding that PMCA could interact with several specific signaling proteins, it was concluded that its location in defined sites of the cell membrane could be a prerequisite for efficient intercellular communication.

17

Regulation of mountain streams versus ecological balance as illustrated by the example of the upper Vistula basin (part I)

75%

Niechwiej Sj A.

Przegląd Naukowy. Inżynieria i Kształtowanie Środowiska

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2015

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tom 24

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nr 3(69)

18

Placing plant protection products on the Polish market with regard to the registration of individual formulations

75%

Matyjaszczyk E.

Annales Universitatis Mariae Curie-Skłodowska. Sectio E. Agricultura

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2008

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tom 63

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nr 2

19

Regulation of nuclear phospholipase C activity

75%

Manzoli L., Billi A. M., Martelli A. M., Cocco L.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

A body of evidence, linking inositide-specific phospholipase C (PI-PLC) to the nucleus, is quite extensive. The main isoform in the nucleus is PI-PLQCß1, whose activity is up-regulated in response to insulin-like growth factor-1 (IGF-1) or insulin stimulation. Whilst at the plasma membrane this PI-PLC is activated and regulated by Gaq/a11 and Gßy subunits, there is yet no evidence that qa/a11 is present within the nuclear compartment, neither GTP-y-S nor AlF4 can stimulate PI-PLCß1 activity in isolated nuclei. Here we review the evidence that upon occupancy of type 1 IGF receptor there is translocation to the nucleus of phosphorylated mitogen-activated protein kinase (MAPK) which phosphorylates nuclear PI-PLCß1 and triggers its signalling, hinting at a separate pathway of regulation depending on the subcellular location of PI-PLCß1. The difference in the regulation of the activity of PI-PLCß1 mirrors the evidence that nuclear and cytoplasmatic inositides can differ markedly in their signalling capability. Indeed, we do know that agonists which affect nuclear inositol lipid cycle at the nucleus do not stimulate the one at the plasma membrane.

20

The ghrelin pentapeptide inhibits the secretion of pancreatic juice in rats

75%

Kapica M., Laubitz D., Puzio I., Jankowska A., Zabielski R.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

Ghrelin, a 28 amino acids polypeptide was recognized as an endogenous ligand for the growth hormone secretagogue receptor. It turned out that the entire sequence of ghrelin is not necessary for performing the above-mentioned functions. It was suggested that 5 residues (Gly-Ser-Ser(n-octanoyl)-Phe, pentaghrelin) constituted functionally active part of the full-length polypeptide. Ghrelin-28 was found to inhibit pancreatic enzyme output in rats, though the effect of pentaghrelin was not studied so far. The study aimed to determine the involvement of pentaghrelin in pancreatic juice secretion in anaesthetized rats. Male Wistar rats (220 ± 20 g body weight, b. wt.) were anesthetized, the external jugular vein and common biliary-pancreatic duct were cannulated. Pentaghrelin boluses (iv, 1.2, 12, and 50 nmol kg-1 b. wt.) were injected every 30 min with or without CCK-8 infusion, duodenal mucosal CCK1 receptor blockade with tarazepide, vagotomy and capsaicin pretreatment. Pentaghrelin boluses reduced the volume of pancreatic-biliary juice, protein and trypsin outputs both under basal and CCK-8-stimulated conditions in a dose-dependent manner. However, exogenous pentaghrelin failed to affect the pancreatic secretion in rats subjected to vagotomy, capsaicin deactivation of afferents or pretreatment with Tarazepide. In conclusion, pentaghrelin may control exocrine pancreas secretion by affecting duodenal neurohormonal mechanism(s) involving CCK and vagal nerves in rats.

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