Sudomoina M.A.,Moscow State University |
Sukhinina T.S.,Russian Cardiology Scientific and Production Center |
Barsova R.M.,Moscow State University |
Favorov A.V.,State Research Center Gosgenetika |
And 8 more authors.
Molecular Biology | Year: 2010
Frequencies of the carriership of alleles and genotypes of functionally important polymorphous loci of some inflammation genes (proinflammatory cytokine genes IL-6, LTA, and TNF; anti-inflammatory cytokine gene TGFB1; and CC chemokine receptor 5 gene CCR5) were analyzed in 199 ethnic Russian patients with myocardial infarction (MI) and in a control group of 142 persons of the same ethnic descent. Complex analysis by the APSampler algorithm revealed associations of MI with the carriership of all polymorphic variants either regarded as individual risk factors (insertion-deletion polymorphism of CCR5 and SNP G252A LTA) or in combination with other alleles or genotypes. The carriership of bi-or triallelic combinations was associated with MI more reliable than the carriership of any subsets: single alleles or allele pairs. The protective triallelic combination d*CCR5 + 252G*LTA + -174C*Il-6 was found to be the most significant (p = 0.0006, OR = 0.23, CI = 0.090-0.56). Separate analysis of genetic susceptibility to MI in men and women demonstrated sexual dimorphism for the CCR5 gene. © 2010 Pleiades Publishing, Ltd.
Proshkin S.A.,State Research Center Gosgenetika |
Mironov A.S.,State Research Center Gosgenetika
Molecular Biology | Year: 2011
The elongation complex, which involves RNA polymerase, a DNA template, and nascent RNA, is a central intermediate in the transcription cycle. It is the elongation complex that represents the main target for different regulatory factors. Ample structural and biochemical data were obtained in the past several years to shed light upon the molecular details of the RNA polymerase function. Cooperation between the RNA polymerase elongation complex and the translating ribosome was established recently. The review discusses the mechanisms regulating bacterial transcription elongation. © 2011 Pleiades Publishing, Ltd.
Zavilgelsky G.B.,State Research Center Gosgenetika |
Kotova V.Y.,State Research Center Gosgenetika
Molecular Biology | Year: 2014
The Ocr antirestriction protein, which is encoded by bacteriophage T7 0.3 (ocr), specifically inhibits type I restriction-modification enzymes. Ocr belongs to a family of DNA-mimicking proteins. Native Ocr forms homodimers both in solution and in crystal. Ocr mutants with two amino acid substitutions (Orc F53D A57E and Ocr F53R V77D) were constructed to occur as monomers in solution. The dissociation constant K d for the Ocr complex with EcoKI (R2M2S) proved to differ by three orders of magnitude between the (Ocr)2 dimer and Ocr F53D A57E and Ocr F53R V77D monomers (10-10 M vs. 10-7 M). Antimodification activity was substantially lower in the Ocr monomers. The dimeric form found to be essential for high inhibitory activity of Ocr. © 2014 Pleiades Publishing, Inc.
Polymorphic markers Ala455Val of the THBD gene and Arg353Gln of the F7 gene and genetic association with unfavorable outcomes of coronary atherosclerosis in patients with a history of acute ischemic heart disease
Pushkov A.A.,State Research Center Gosgenetika |
Blagodatskikh K.A.,State Research Center Gosgenetika |
Nikitin A.G.,State Research Center Gosgenetika |
Agapkina Y.V.,State Research Center Gosgenetika |
And 27 more authors.
Russian Journal of Genetics | Year: 2011
The polymorphic markers Ala455Val of the THBD gene and Arg353Gln of the F7 gene were tested for association with the frequency of unfavorable outcomes in patients with a history of acute ischemic heart disease. The study involved 1145 patients hospitalized in cardiology clinics of Moscow, St. Petersburg, Kazan, Chelyabinsk, Perm, Stavropol, and Rostov-on-Don because of acute ischemic heart disease. The patients were followed up for up to 62.5 months. None of the markers displayed a significant association with the time to an endpoint. The patients were then grouped by sex. In females, the frequency of unfavorable outcomes (fatal or nonfatal myocardial infarction and fatal or nonfatal stroke) was higher in carriers of allele Val of the Ala344Val polymorphic marker of the THBD gene and carriers of genotype Arg/Arg of the Arg353Gln polymorphic marker of the F7 gene, but the difference was not statistically significant. Such an increase in frequency was not observed in males. To study the combined effect of the polymorphic markers of the THBD and F7 genes, the course of ischemic heart disease was compared for two female subgroups. One included carriers of allele Val of the Ala344Val polymorphic marker of the THBD gene and genotype Arg/Arg of the Arg353Gln polymorphic marker of the F7 gene; the other subgroup included carriers of genotype Ala/Ala of the Ala455Val polymorphic marker of the THBD gene and allele Gln of the Arg353Gln polymorphic marker of the F7 gene. The frequency of unfavorable outcomes in the first subgroup was higher than in the second one. The time to an endpoin was 40.5 months (95% confidence interval (CI) 33.5-47.6) in the first subgroup and 51.6 months (95% CI 45.0-58.1) in the second subgroup (χ 2 = 4.15, P = 0.042). The results made it possible to assume that the F7 and THBD genes play an important role in genetic predisposition to unfavorable outcomes in patients with a history of acute ischemic heart disease. © 2011 Pleiades Publishing, Inc.
Mel'kina O.E.,State Research Center Gosgenetika |
Manukhov I.V.,State Research Center Gosgenetika |
Zavilgelsky G.B.,State Research Center Gosgenetika
Molecular Biology | Year: 2010
The Vibrio fischeri luxICDABEG genes are upregulated by the autoinducer N-(3-oxohexanoyl) L-homoserine lactone and the LuxR protein. The latter contains 250 aa and consists of two domains. The C-terminal domain, which extends from approximately residue 162 to the C end, is thought to bind lux regulatory DNA and activate transcription of the luxICDABEG genes. The N-terminal domain, which binds the autoinducer, comprises approximately 70% of LuxR residues. In Escherichia coli, the C-terminal domain can activate lux genes with the absence of the autoinducer. Previously, it was shown that the ATP-dependent Lon protease of E. coli was involved in the downregulation of the V. fischeri lux operon and that LuxR was a target of Lon protease. Effects of Lon protease on V. fischeri luxICDABEG gene expression are compared in this study in model plasmids with lux operon genes or DNA fragments encoding either full-length LuxR or its C-terminal domain. It is shown that full-length LuxR, but not C-terminal domain is a target protein for Lon protease. The full-length LuxR protein is a more potent activator than its C-terminal domain. It displays upregulating activity at intracellular concentrations approximately two orders of magnitude lower than its C-terminal domain. © 2010 Pleiades Publishing, Ltd.