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6. CobB1 deacetylase activity in Streptomyces coelicolor

Author

Mikulik, Karel, Felsberg, Jurgen, Kudrnacova, Eva, Bezouskova, Silvia, Setinova, Dita, Stodulkova, Eva, Zidkova, Jarmila, and Zidek, Vaclav

Subjects
Streptomyces -- Physiological aspects -- Health aspects, Biological sciences
Abstract

Silent information regulators are [NAD.sup.+]-dependent enzymes that display differential specificity toward acetylated substrates. This report provides first evidence for deacetylation activity of CobB1 in Streptomyces coelicolor. The protein is highly conserved in streptomycetes. The CobB1 protein catalytically removes the acetyl group from acetylated bovine serum albumin. In the absence of [NAD.sup.+] or when [NAD.sup.+] was substituted with nicotinamide, deacetylation was stopped. We isolated gene encoding AcetylCoA synthetaseA. The recombinant enzyme produces Acetyl-CoA from acetate. The highest acsA-mRNA level was detected in cells from the exponential phase of growth, and then decreased in transition and stationary phases of growth. Acetylated acsA loses the ability to transfer acetate to CoA. Deacetylation of the enzyme required CobB1, [ATP-Mg.sup.2], and [NAD.sup.+]. Using specific antibodies against acetylated lys, CobB1, and acsA, we found relationship between level of CobB1 and acetylation of acsA, indicating that CobB1 is involved in regulating the acetylation level of acsA and consequently its activity. It was found that 1-acetyl-tetrahydroxy and 1-acetyl pentahydroxy antraquinone inhibit the deacetylation activity of CobB1. Key words: sirtuin, [NAD.sup.+]dependent deacetylation activity CobB1, Streptomyces coeliocolor, AcetylCoA synthetaseA. Les regulateurs d'information silencieux sont des enzymes dependantes du [NAD.sup.+] qui montrent une specificite differentielle envers les substrats acetyles. Cet article demontre pour la premiere fois que CobB1 possede une activite desacetylase chez Streptomyces coelicolor. La proteine est hautement conservee chez streptomyces et possede un repliement de Rossmann et un module de liaison de zinc caracteristiques. La proteine CobB1 de S. coelicolor a ete exprimee chez Escherichia coli et purifiee. L'enzyme purifiee enleve de facon catalytique le groupement acetyle de l'albumine serique bovine acetylee. En absence de [NAD.sup.+] ou lorsque le [NAD.sup.+] etait remplace par le nicotinamide, la desacetylation s'arretait. Nous avons examine l'expression de l'acetyl-CoA synthase (acsA), une enzyme metabolique, et determine si l'enzyme pouvait aussi etre regulee par acetylation et activee par desacetylation par CobB1. L'activite la plus elevee de l'acsA etait detectee chez les cellules en croissance exponentielle, et l'activite de l'enzyme diminuait lors de la phase de transition. En phase stationnaire, l'activite de l'enzyme augmentait de 60 % par rapport a la valeur trouvee dans les preparations en phase exponentielle. L'acsA acetylee perdait sa capacite de transferer l'acetate a la CoA. La desacetylation de l'enzyme requerait CobB1, du [Mg.sup.2+]-ATP et du [NAD.sup.+]. Une relation entre le niveau de CobB1 et l'acetylation de l'acsA a ete trouvee grace a des anticorps specifiques diriges contre la lys acetylee, CobB1 et l'acsA, indiquant que CobB1 est impliquee dans la regulation des niveaux d'acetylation de l'acsA et consequemment de son activite. Nous avons trouve que la 1-acetyl-tetrahydroxy et la 1-acetyl-pentahydroxy antraquinone sont de puissants inhibiteurs de l'activite desacetylase de CobB1. Mots-cles : CobB1, desacetylation dependante du [NAD.sup.+], Streptomyces coelicolor), acetyl-CoA synthase (acsA). [Traduit par la Redaction], Introduction The silent informational regulators (sirtuins) are proteins found in all organisms from bacteria to humans. The number of sirtuin family proteins correlates with the increasing level of species diversification [...]

Published
2012
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7. Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function

Author

McDermott-Roe, Chris, Ye, Junmei, Ahmed, Rizwan, Sun, Xi-Ming, Serafin, Anna, Ware, James, Bottolo, Leonardo, Muckett, Phil, Canas, Xavier, Zhang, Jisheng, Rowe, Glenn C., Buchan, Rachel, Lu, Han, Braithwaite, Adam, Mancini, Massimiliano, Hauton, David, Marti, Ramon, Garcia-Arumi, Elena, Hubner, Norbert, Jacob, Howard, Serikawa, Tadao, Zidek, Vaclav, Papousek, Frantisek, Kolar, Frantisek, Cardona, Maria, Ruiz-Meana, Marisol, Garcia-Dorado, David, Comella, Joan X., Felkin, Leanne E., Barton, Paul J.R., Arany, Zoltan, Pravenec, Michal, Petretto, Enrico, Sanchis, Daniel, and Cook, Stuart A.

Subjects
Nucleases -- Physiological aspects -- Research, Mitochondria -- Genetic aspects -- Physiological aspects -- Research, Heart enlargement -- Risk factors -- Diagnosis -- Genetic aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Left ventricular mass (LVM) is a highly heritable trait (1) and an independent risk factor for all-cause mortality (2). So far, genomewide association studies have not identified the genetic factors that underlie LVM variation (3), and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood (4,5). Unbiased systems genetics approaches in the rat (6,7) now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis (8) but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-α and PGC1a (which are master regulators of mitochondrial and cardiac function) (9-11), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endogin maladaptive cardiac hypertrophy., Increased LVM is a clinically important trait that independently predicts the risk of heart failure, sudden death and all-cause mortality (2). Although LVM is a heritable complex trait (1), large [...]

Published
2011
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13. Nuclear transport of nicotinamide phosphoribosyltransferase is cell cycle–dependent in mammalian cells, and its inhibition slows cell growth

Author

Svoboda, Petr, primary, Krizova, Edita, additional, Sestakova, Sarka, additional, Vapenkova, Kamila, additional, Knejzlik, Zdenek, additional, Rimpelova, Silvie, additional, Rayova, Diana, additional, Volfova, Nikol, additional, Krizova, Ivana, additional, Rumlova, Michaela, additional, Sykora, David, additional, Kizek, Rene, additional, Haluzik, Martin, additional, Zidek, Vaclav, additional, Zidkova, Jarmila, additional, and Skop, Vojtech, additional

Published
2019
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15. Knockout of DAPIT protein disrupts ATP synthase oligomerisation and has a profound role in regulation of glucose homeostasis

Author

Mracek, Tomas, primary, Pecina, Petr, additional, Nuskova, Hana, additional, Kovalcikova, Jana, additional, Pecinova, Alena, additional, Alan, Lukas, additional, Rodinova, Marie, additional, Zidek, Vaclav, additional, Landa, Vladimir, additional, Kaplanova, Vilma, additional, Kolar, Frantisek, additional, Papousek, Frantisek, additional, Habart, David, additional, Kazdova, Ludmila, additional, Bardova, Kristyna, additional, Tauchmannova, Katerina, additional, Drahota, Zdenek, additional, Kopecky, Jan, additional, Pravenec, Michal, additional, and Houstek, Josef, additional

Published
2018
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17. Nrf2-Mediated Antioxidant Defense and Peroxiredoxin 6 Are Linked to Biosynthesis of Palmitic Acid Ester of 9-Hydroxystearic Acid

Author

Kuda, Ondrej, primary, Brezinova, Marie, additional, Silhavy, Jan, additional, Landa, Vladimir, additional, Zidek, Vaclav, additional, Dodia, Chandra, additional, Kreuchwig, Franziska, additional, Vrbacky, Marek, additional, Balas, Laurence, additional, Durand, Thierry, additional, Hübner, Norbert, additional, Fisher, Aron B., additional, Kopecky, Jan, additional, and Pravenec, Michal, additional

Published
2018
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18. Direct linkage of mitochondrial genome variation to risk factors for type 2 diabetes in conplastic strains

Author

Pravenec, Michal, Hyakukoku, Masaya, Houstek, Josef, Zidek, Vaclav, Landa, Vladimir, Mlejnek, Petr, Miksik, Ivan, Dudova-Mothejzikova, Kristyna, Pecina, Petr, Vrbacky, Marek, Drahota, Zdenek, Vojtiskova, Alena, Kazdova, Ludmila, Mracek, Tomas, Oliyarnyk, Olena, Ho, Christopher, Qi, Nathan, Ken Sugimoto, Jiaming Wang, and Kurtz, Theodore

Subjects
Type 2 diabetes -- Risk factors, Linkage (Genetics) -- Observations, Biological diversity -- Analysis, Mitochondria -- Analysis, Health
Abstract

The study results from conplastic strains of rat model which provide evidence linking naturally occurring variation in the mitochondrial genome, independent of variation in the nuclear genome and other confounding factors, to inherited variation in known risk factors for type 2 diabetes is presented.

Published
2007

21. Transposon‐mediated transgenesis, transgenic rescue, and tissue‐specific gene expression in rodents and rabbits

Author

Katter, Katharina, primary, Geurts, Aron M., additional, Hoffmann, Orsolya, additional, Mátés, Lajos, additional, Landa, Vladimir, additional, Hiripi, László, additional, Moreno, Carol, additional, Lazar, Jozef, additional, Bashir, Sanum, additional, Zidek, Vaclav, additional, Popova, Elena, additional, Jerchow, Boris, additional, Becker, Katja, additional, Devaraj, Anantharam, additional, Walter, Ingrid, additional, Grzybowksi, Michael, additional, Corbett, Molly, additional, Filho, Artur Rangel, additional, Hodges, Matthew R., additional, Bader, Michael, additional, Ivics, Zoltán, additional, Jacob, Howard J., additional, Pravenec, Michal, additional, Bősze, Zsuzsanna, additional, Rülicke, Thomas, additional, and Izsvák, Zsuzsanna, additional

Published
2012
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23. Dissection of Chromosome 18 Blood Pressure and Salt-Sensitivity Quantitative Trait Loci in the Spontaneously Hypertensive Rat

Author

Johnson, Michelle D., primary, He, Liqun, additional, Herman, Daniel, additional, Wakimoto, Hiroko, additional, Wallace, Caroline A., additional, Zidek, Vaclav, additional, Mlejnek, Petr, additional, Musilova, Alena, additional, Simakova, Miroslava, additional, Vorlicek, Jaroslav, additional, Kren, Vladimir, additional, Viklicky, Ondrej, additional, Qi, Nathan R., additional, Wang, Jiaming, additional, Seidman, Christine E., additional, Seidman, Jonathan, additional, Kurtz, Theodore W., additional, Aitman, Timothy J., additional, and Pravenec, Michal, additional

Published
2009
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24. Identification of renal Cd36 as a determinant of blood pressure and risk for hypertension

Author

Pravenec, Michal, primary, Churchill, Paul C, additional, Churchill, Monique C, additional, Viklicky, Ondrej, additional, Kazdova, Ludmila, additional, Aitman, Timothy J, additional, Petretto, Enrico, additional, Hubner, Norbert, additional, Wallace, Caroline A, additional, Zimdahl, Heike, additional, Zidek, Vaclav, additional, Landa, Vladimir, additional, Dunbar, Joseph, additional, Bidani, Anil, additional, Griffin, Karen, additional, Qi, Nathan, additional, Maxova, Martina, additional, Kren, Vladimir, additional, Mlejnek, Petr, additional, Wang, Jiaming, additional, and Kurtz, Theodore W, additional

Published
2008
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26. Identification of Mutated Srebf1 as a QTL Influencing Risk for Hepatic Steatosis in the Spontaneously Hypertensive Rat

Author

Pravenec, Michal, primary, Kazdova, Ludmila, additional, Landa, Vladimir, additional, Zidek, Vaclav, additional, Mlejnek, Petr, additional, Simakova, Miroslava, additional, Jansa, Petr, additional, Forejt, Jiri, additional, Kren, Vladimir, additional, Krenova, Drahomira, additional, Qi, Nathan, additional, Wang, Jia-Ming, additional, Chan, Derrick, additional, Aitman, Timothy J., additional, and Kurtz, Theodore W., additional

Published
2008
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29. Integrated transcriptional profiling and linkage analysis for identification of genes underlying disease

Author

Hubner, Norbert, primary, Wallace, Caroline A, additional, Zimdahl, Heike, additional, Petretto, Enrico, additional, Schulz, Herbert, additional, Maciver, Fiona, additional, Mueller, Michael, additional, Hummel, Oliver, additional, Monti, Jan, additional, Zidek, Vaclav, additional, Musilova, Alena, additional, Kren, Vladimir, additional, Causton, Helen, additional, Game, Laurence, additional, Born, Gabriele, additional, Schmidt, Sabine, additional, Müller, Anita, additional, Cook, Stuart A, additional, Kurtz, Theodore W, additional, Whittaker, John, additional, Pravenec, Michal, additional, and Aitman, Timothy J, additional

Published
2005
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32. Y-Chromosome Transfer Induces Changes in Blood Pressure and Blood Lipids in SHR

Author

Kren, Vladimir, primary, Qi, Nianning, additional, Krenova, Drahomira, additional, Zidek, Vaclav, additional, Sladká, Milada, additional, Jáchymová, Marie, additional, Míková, Blanka, additional, Horky, Karel, additional, Bonne, Anita, additional, Van Lith, Hein A., additional, Van Zutphen, Bert F. M., additional, Lau, Yun-Fai Chris, additional, Pravenec, Michal, additional, and St. Lezin, Elizabeth, additional

Published
2001
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33. Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats

Author

Pravenec, Michal, primary, Landa, Vladimir, additional, Zidek, Vaclav, additional, Musilova, Alena, additional, Kren, Vladimir, additional, Kazdova, Ludmila, additional, Aitman, Timothy J., additional, Glazier, Anne M., additional, Ibrahimi, Azeddine, additional, Abumrad, Nada A., additional, Qi, Nianning, additional, Wang, Jia-Ming, additional, St. Lezin, Elizabeth M., additional, and Kurtz, Theodore W., additional

Published
2001
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38. Genetic Isolation of a Chromosome 1 Region Affecting Susceptibility to Hypertension-Induced Renal Damage in the Spontaneously Hypertensive Rat

Author

St. Lezin, Elizabeth, primary, Griffin, Karen A., additional, Picken, Maria, additional, Churchill, Monique C., additional, Churchill, Paul C., additional, Kurtz, Theodore W., additional, Liu, Weizhong, additional, Wang, Ning, additional, Kren, Vladimir, additional, Zidek, Vaclav, additional, Pravenec, Michal, additional, and Bidani, Anil K., additional

Published
1999
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39. Effect of Chromosome 19 Transfer on Blood Pressure in the Spontaneously Hypertensive Rat

Author

St. Lezin, Elizabeth, primary, Zhang, Lei, additional, Yang, Ying, additional, Wang, Jia-Ming, additional, Wang, Ning, additional, Qi, Nianing, additional, Steadman, J. Sanford, additional, Liu, Weizhong, additional, Kren, Vladimir, additional, Zidek, Vaclav, additional, Krenova, Drahomira, additional, Churchill, Paul C., additional, Churchill, Monique C., additional, and Pravenec, Michal, additional

Published
1999
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42. Quantitative trait loci for cellular defects in glucose and fatty acid metabolism in hypertensive rats

Author

Aitman, Timothy J., primary, Gotoda, Takanari, additional, Evans, Alison L., additional, Imrie, Helen, additional, Heath, Karen E., additional, Trembling, Paul M., additional, Truman, Hazel, additional, Wallace, Caroline A., additional, Rahman, Ahmadur, additional, Doré, Caroline, additional, Flint, Jonathan, additional, Kren, Vladimir, additional, Zidek, Vaclav, additional, Kurtz, Theodore W., additional, Pravenec, Michal, additional, and Scott, James, additional

Published
1997
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43. Transposon-mediated transgenesis, transgenic rescue, and tissue-specific gene expression in rodents and rabbits.

Author

Katter, Katharina, Geurts, Aron M., Hoffmann, Orsolya, Mátés, Lajos, Landa, Vladimir, Hiripi, László, Moreno, Carol, Lazar, Jozef, Bashir, Sanum, Zidek, Vaclav, Popova, Elena, Jerchow, Boris, Becker, Katja, Devaraj, Anantharam, Walter, Ingrid, Grzybowksi, Michael, Corbett, Molly, Filho, Artur Rangel, Hodges, Matthew R., and Bader, Michael

Subjects
GENE expression, MOLECULAR genetics, RABBITS, LEPORIDAE, RODENTS
Abstract

Germline transgenesis is an important procedure for functional investigation of biological pathways, as well as for animal biotechnology. We have established a simple, nonviral protocol in three important biomedical model organisms frequently used in physiological studies. The protocol is based on the hyperactive Sleeping Beauty transposon system, SB100X, which reproducibly promoted generation of transgenic founders at frequencies of 50-64, 14-72, and 15% in mice, rats, and rabbits, respectively. The SB100X-mediated transgene integrations are less prone to genetic mosaicism and gene silencing as compared to either the classical pronuclear injection or to lentivirus-mediated transgenesis. The method was successfully applied to a variety of transgenes and animal models, and can be used to generate founders with single-copy integrations. The transposon vector also allows the generation of transgenic lines with tissue-specific expression patterns specified by promoter elements of choice, exemplified by a rat reporter strain useful for tracking serotonergic neurons. As a proof of principle, we rescued an inborn genetic defect in the fawn-hooded hypertensive rat by SB100X transgenesis. A side-by-side comparison of the SB100X- and piggyBac-based protocols revealed that the two systems are complementary, offering new opportunities in genome manipulation. [ABSTRACT FROM AUTHOR]

Published
2013
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44. A spontaneous mutation in the desmoglein 4 gene underlies hypotrichosis in a newlanceolate hairrat model.

Author

Meyer, Birgit, Bazzi, Hisham, Zidek, Vaclav, Musilova, Alena, Pravenec, Michal, Kurtz, Theodore W., Nurnberg, Peter, and Christiano, Angela M.

Subjects
GENETIC mutation, GENES, RATS, CHROMOSOMES, HUMAN chromosomes, HISTOLOGY
Abstract

A recessive hairless mutation arose spontaneously in a congenic line of spontaneously hypertensive rats SHR.BN-(D1Mit3-Igf2)/Ipcv. The mutant rats develop generalized alopecia except for partial hair growth on their heads. Affected animals of the congenic line were crossed with LEW rats and randomly bred for several generations. A genome scan in 74 affected and 75 unaffected offspring localized the mutant gene on rat chromosome 18p12, near the marker D18Rat107, which is closely linked to the desmosomal cadherin gene cluster, syntenic to mouse chromosome 18 and human chromosome 18q12. Recently, the mouse and rat phenotypeslah/lah(lanceolate hair) andlahJ/lahJ(lanceolate hair-J) were found to be caused by mutations in the desmoglein 4 (Dsg4) gene. Direct sequencing of theDsg4gene in the SHR revealed a homozygous C-to-T transition generating a premature termination codon within exon 8 in the affected animals. Further studies on the skin histology in affected rats demonstrated features consistent with alanceolate hairmutation, providing further support for the crucial role of desmoglein 4 in hair shaft differentiation. [ABSTRACT FROM AUTHOR]

Published
2004
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45. Genetic Map of AFLP Markers in the Rat (Rattus norvegicus) Derived From the H x B/Ipcv and B x H/Cub Sets of Recombinant Inbred Strains.

Author

Bonne, Anita C.M., den Bieman, Maria G., Gillissen, Gert F., Kren, Vladimir, Krenova, Drahomira, Bila, Vlasta, Zidek, Vaclav, Kostka, Vlastimil, Musilova, Alena, Pravenec, Michal, van Zutphen, Bert F.M., and van Lith, Hein A.

Subjects
GENETIC polymorphisms, RATS, INBREEDING
Abstract

The amplified fragment length polymorphism (AFLP) technique has been used to enhance marker density in a large set of recombinant inbred strains (H × B and B × H) derived from a spontaneously hypertensive rat (SHR/OlaIpcv) and a Brown-Norway (BN.1x/Cub) inbred strain. Thirteen different primer combinations were tested and a total of 191 polymorphic bands were detected. From these polymorphic bands 89 AFLP markers could be assigned to specific chromosomes. Several of these AFLP markers were mapped to regions with low marker density, thus filling up gaps in the existing genetic map of these recombinant inbred strains. These results substantiate the value of the AFLP technology in increasing marker density in genetic maps. [ABSTRACT FROM AUTHOR]

Published
2003

46. Pharmacogenetic evidence that cd36 is a key determinant of the metabolic effects of pioglitazone.

Author

Qi, Nianning, Kazdova, Ludmila, Zidek, Vaclav, Landa, Vladimir, Kren, Vladimir, Pershadsingh, Harrihar A, Lezin, Elizabeth St, Abumrad, Nada A, Pravenec, Michal, and Kurtz, Theodore W

Abstract

Pioglitazone, like other thiazolidinediones, is an insulin-sensitizing agent that activates the peroxisome proliferator-activated receptor gamma and influences the expression of multiple genes involved in carbohydrate and lipid metabolism. However, it is unknown which of these many target genes play primary roles in determining the antidiabetic and hypolipidemic effects of thiazolidinediones. To specifically investigate the role of the Cd36 fatty acid transporter gene in the insulin-sensitizing actions of thiazolidinediones, we studied the metabolic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a deletion mutation in Cd36 in comparison to congenic and transgenic strains of SHR that express wild-type Cd36. In congenic and transgenic SHR with wild-type Cd36, administration of pioglitazone was associated with significantly lower circulating levels of fatty acids, triglycerides, and insulin as well as lower hepatic triglyceride levels and epididymal fat pad weights than in SHR harboring mutant Cd36. Additionally, insulin-stimulated glucose oxidation in isolated soleus muscle was significantly augmented in pioglitazone-fed rats with wild-type Cd36 versus those with mutant Cd36. The Cd36 genotype had no effect on pioglitazone-induced changes in blood pressure. These findings provide direct pharmacogenetic evidence that in the SHR model, Cd36 is a key determinant of the insulin-sensitizing actions of a thiazolidinedione ligand of peroxisome proliferator-activated receptor gamma.

Published
2002
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