ГЕНЕТИКА ВОСПРИИМЧИВОСТИ К ГЕЛЬМИНТОЗАМ У ЧЕЛОВЕКА

Objective of research: to provide the analysis of literature sources describing the in uence of host genes on genetic susceptibility to helminthiasis and the features of its pathogenesis. Results and discussion: all recent scienti c works dedicated to the in uence of host genes on genetic susceptibility to helminthiasis and the features of its pathogenesis were considered. The most important determinants of impact of host genes on genetic susceptibility to helminthiasis are gene polymorphisms TAP for echinococcosis, variants of genetic loci SM1 and SM2 for bilharziasis (schistosomiasis), and gene polymorphisms HLA for all three parasitic diseases described in this article.Цель исследования – дать анализ имеющихся в литературе работ, посвященных изучению влияния генов хозяина на генетическую восприимчивость к гельминтозам и на особенности их патогенеза.Проанализированы все работы за последнее время, посвященные влиянию генов хозяина на генетическую восприимчивость к гельминтозам и на особенности их патогенеза. Наиболее важными детерминантами влияния генов хозяина на генетическую восприимчивость к гельминтозам являются полиморфизмы генов TAP для эхинококкоза, варианты генных локусов SM1 и SM2 для шистосомоза и полиморфизмы генов HLA для всех трех рассмотренных в статье паразитарных болезней.

FISH mapping of Philadelphia negative BCR/ABL1 positive CML

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Effects of a recombinant gene expression on ColE1-like plasmid segregation in Escherichia coli

<p>Abstract</p> <p>Background</p> <p>Segregation of expression plasmids leads to loss of recombinant DNA from transformed bacterial cells due to the irregular distribution of plasmids between the daughter cells during cell division. Under non-selective conditions this segregational instability results in a heterogeneous population of cells, where the non-productive plasmid-free cells overgrow the plasmid-bearing cells thus decreasing the yield of recombinant protein. Amongst the factors affecting segregational plasmid instability are: the plasmid design, plasmid copy-number, host cell genotype, fermentation conditions etc. This study aims to investigate the influence of transcription and translation on the segregation of recombinant plasmids designed for constitutive gene expression in <it>Escherichia coli </it>LE392 at glucose-limited continuous cultivation. To this end a series of pBR322-based plasmids carrying a synthetic human interferon-gamma (hIFNγ) gene placed under the control of different regulatory elements (promoter and ribosome-binding sites) were used as a model.</p> <p>Results</p> <p>Bacterial growth and product formation kinetics of transformed <it>E. coli </it>LE392 cells cultivated continuously were described by a structured kinetic model proposed by Lee et al. (1985). The obtained results demonstrated that both transcription and translation efficiency strongly affected plasmid segregation. The segregation of plasmid having a deleted promoter did not exceed 5% after 190 h of cultivation. The observed high plasmid stability was not related with an increase in the plasmid copy-number. A reverse correlation between the yield of recombinant protein (as modulated by using different ribosome binding sites) and segregational plasmid stability (determined by the above model) was also observed.</p> <p>Conclusions</p> <p>Switching-off transcription of the hIFNγ gene has a stabilising effect on ColE1-like plasmids against segregation, which is not associated with an increase in the plasmid copy-number. The increased constitutive gene expression has a negative effect on segregational plasmid stability. A kinetic model proposed by Lee et al. (1985) was appropriate for description of <it>E. coli </it>cell growth and recombinant product formation in chemostat cultivations.</p

The 3′ Untranslated Regions of Influenza Genomic Sequences Are 5′PPP-Independent Ligands for RIG-I

Retinoic acid inducible gene-I (RIG-I) is a key regulator of antiviral immunity. RIG-I is generally thought to be activated by ssRNA species containing a 5′-triphosphate (PPP) group or by unphosphorylated dsRNA up to ∼300 bp in length. However, it is not yet clear how changes in the length, nucleotide sequence, secondary structure, and 5′ end modification affect the abilities of these ligands to bind and activate RIG-I. To further investigate these parameters in the context of naturally occurring ligands, we examined RNA sequences derived from the 5′ and 3′ untranslated regions (UTR) of the influenza virus NS1 gene segment. As expected, RIG-I-dependent interferon-β (IFN-β) induction by sequences from the 5′ UTR of the influenza cRNA or its complement (26 nt in length) required the presence of a 5′PPP group. In contrast, activation of RIG-I by the 3′ UTR cRNA sequence or its complement (172 nt) exhibited only a partial 5′PPP-dependence, as capping the 5′ end or treatment with CIP showed a modest reduction in RIG-I activation. Furthermore, induction of IFN-β by a smaller, U/A-rich region within the 3′ UTR was completely 5′PPP-independent. Our findings demonstrated that RNA sequence, length, and secondary structure all contributed to whether or not the 5′PPP moiety is needed for interferon induction by RIG-I

Interaction of SET domains with histones and nucleic acid structures in active chromatin

Changes in the normal program of gene expression are the basis for a number of human diseases. Epigenetic control of gene expression is programmed by chromatin modifications—the inheritable “histone code”—the major component of which is histone methylation. This chromatin methylation code of gene activity is created upon cell differentiation and is further controlled by the “SET” (methyltransferase) domain proteins which maintain this histone methylation pattern and preserve it through rounds of cell division. The molecular principles of epigenetic gene maintenance are essential for proper treatment and prevention of disorders and their complications. However, the principles of epigenetic gene programming are not resolved. Here we discuss some evidence of how the SET proteins determine the required states of target genes and maintain the required levels of their activity. We suggest that, along with other recognition pathways, SET domains can directly recognize the nucleosome and nucleic acids intermediates that are specific for active chromatin regions

GENETICS OF SUSCEPTIBILITY TO HUMAN HELMINTHIASIS

Objective of research: to provide the analysis of literature sources describing the in uence of host genes on genetic susceptibility to helminthiasis and the features of its pathogenesis. Results and discussion: all recent scienti c works dedicated to the in uence of host genes on genetic susceptibility to helminthiasis and the features of its pathogenesis were considered. The most important determinants of impact of host genes on genetic susceptibility to helminthiasis are gene polymorphisms TAP for echinococcosis, variants of genetic loci SM1 and SM2 for bilharziasis (schistosomiasis), and gene polymorphisms HLA for all three parasitic diseases described in this article