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1

Is tRNA only a translation factor or also a regulator of other processes?

100%
Wegrzyn G., Wegrzyn A.
Journal of Applied Genetics
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2008
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vol. 49
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issue 1
115-122
EN
Abstract. tRNA has been discovered as a factor playing a central role in the translation of genetic information (encoded in DNA and transcribed to mRNA) into amino acid sequences of proteins. However, subsequent studies led to the hypothesis that during evolution, tRNA originated in replication, not translation. Indeed, there are many examples of tRNA-like molecules playing roles in reactions other than translation, including replication of various replicons. In this review, we have focused on functions of tRNA molecules (not tRNA-like structures) outside of their direct roles in translation as factors for a passive transportation of amino acids into a ribosome and deciphering triplets of nucleotides in codons of mRNA. Interestingly, it appears that such tRNA-dependent reactions are effective only when tRNA is uncharged. The most spectacular examples come from bacterial cells and include induction of the stringent control, regulation of transcription of some operons, and control of replication of ColE1-type plasmids. Recent studies indicated that tRNA (not only pre-tRNA, shown previously to be capable of self-excision of intron sequences) can be responsible for specific cleavage of another transcript, a ColE1 plasmid-encoded RNA I, which is involved in the regulation of plasmid DNA replication initiation. If this reaction is not restricted to RNA I but represents a more general phenomenon, one might suspect a potential role for uncharged tRNA molecules in regulation of various processes, whose efficiency depends on tRNA-cleavable RNAs. This kind of regulation would provide a possibility for a cell to respond to different nutrition conditions resulting in different levels of tRNA aminoacylation.
2

Substrate deprivation therapy: a new hope for patients suffering from neuronopathic forms of inherited lysosomal storage diseases

81%
Jakobkiewicz-Banecka J., Wegrzyn A., Wegrzyn G.
Journal of Applied Genetics
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2007
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vol. 48
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issue 4
383-388
EN
Lysosomal storage diseases are a group of disorders caused by defects in enzymes responsible for degradation of particular compounds in lysosomes. In most cases, these diseases are fatal, and until recently no treatment was available. Introduction of enzyme replacement therapy was a breakthrough in the treatment of some of the diseases. However, while this therapy is effective in reduction of many somatic symptoms, its efficacy in the treatment of the central nervous system is negligible, if any, mainly because of problems with crossing the blood-brain-barrier by intravenously administered enzyme molecules. On the other hand, there are many lysosomal storage diseases in which the central nervous system is affected. Results of very recent studies indicate that in at least some cases, another type of therapy, called substrate deprivation therapy (or substrate reduction therapy) may be effective in the treatment of neuronopathic forms of lysosomal storage diseases. This therapy, based on inhibition of synthesis of the compounds that cannot be degraded in cells of the patients, has been shown to be effective in several animal models of various diseases, and recent reports demonstrate its efficacy in the treatment of patients suffering from Niemann-Pick C disease and Sanfilippo disease.
3

Bacteriophage contamination: is there a simple method to reduce its deleterious effects in laboratory cultures and biotechnological factories?

61%
Los M., Czyz A., Sell E., Wegrzyn A., Neubauer P., Wegrzyn G.
Journal of Applied Genetics
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2004
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vol. 45
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issue 1
111-120
EN
Infection of bacterial cultures by bacteriophages as well as prophage induction in the host cells are serious problems in both research and biotechnological laboratories. Generally, prevention strategies (like good laboratory/factory hygiene, sterilisation, decontamination and disinfection) are necessary to avoid bacteriophage contamination. However, it is well known that no matter how good the laboratory/factory practice and hygiene are, bacteriophage infections occur from time to time. The use of immunised or resistant bacterial strains against specific phages may be helpful, but properties of the genetically modified strains resistant to phages are often worse (from the point of view of a researcher or a biotechnological company) than those of the parental, phage-sensitive strains. In this article we review recent results that may provide a simple way to minimise deleterious effects of bacteriophage infection and prophage induction. It appears that low bacterial growth rates result in a significant inhibition of lytic development of various bacteriophages. Moreover, spontaneous prophage induction is less frequent in slowly growing bacteria.
4

Molecular characterization of Polish patients with familial hypercholesterolemia: novel and recurrent LDLR mutations

42%
Chmara M., Wasag B., Zuk M., Kubalska J., Wegrzyn A., Bednarska-Makaruk M., Pronicka E., Wehr H., Defesche J. C., Rynkiewicz A., Limon J.
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vol. 51
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issue 1
95-106
EN
Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the genes coding for the low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). In this study, a molecular analysis of LDLR and APOB was performed in a group of 378 unrelated ADH patients, to explore the mutation spectrum that causes hypercholesterolemia in Poland. All patients were clinically diagnosed with ADH according to a uniform protocol and internationally accepted WHO criteria. Mutational analysis included all exons, exon-intron boundaries and the promoter sequence of the LDLR, and a fragment of exon 26 of APOB. Additionally, the MLPA technique was applied to detect rearrangements within LDLR. In total, 100 sequence variations were identified in 234 (62%) patients. Within LDLR, 40 novel and 59 previously described sequence variations were detected. Of the 99 LDLR sequence variations, 71 may be pathogenic mutations. The most frequent LDLR alteration was a point mutation p.G592E detected in 38 (10%) patients, followed by duplication of exons 4?8 found in 16 individuals (4.2%). Twenty-five cases (6.6%) demonstrated the p.R3527Q mutation of APOB. Our findings imply that major rearrangements of the LDLR gene as well as 2 point mutations (p.G592E in LDLR and p.R3527Q in APOB) are frequent causes of ADH in Poland. However, the heterogeneity of LDLR mutations detected in the studied group confirms the requirement for complex molecular studies of Polish ADH patients.
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