Incfii
Mostrando 1-12 de 49 artigos, teses e dissertações.
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1. Characterization of the genetic environment of the bla KPC-2 gene among Klebsiella pneumoniae isolates from a Chinese Hospital
Abstract Infection caused by carbapenem-resistant Klebsiella pneumoniae has become a major healthcare threat and KPC-2 enzyme is a dominant factor mediating carbapenems resistance in K. pneumoniae. This study was designed to determine the genetic environment of bla KPC-2, which prevailed in clinical K. pneumoniae isolates recovered in Huashan Hospital, Shang
Braz J Infect Dis. Publicado em: 2016-08
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2. Genética e epidemiologia molecular de enterobactérias produtoras de KPC no Brasil / Genetic and molecular epidemiology of KPC-producing enterobacteria in Brazil.
KPC (Klebsiella pneumoniae carbapenemases) são -lactamases da classe A de Ambler globalmente disseminadas, com 10 variantes, sendo predominates KPC-2 e KPC-3. O objetivo deste trabalho foi estudar a genética e epidemiologia molecular de enterobactérias resistentes aos carbapenêmicos isoladas no Brasil. Sessenta e quatro enterobactérias resistentes aos c
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 14/10/2011
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3. Second replicon in ColV2-K94 mediates the stable coexistence of two incompatible plasmids.
The colicin-producing plasmid pWS12, a Tn903 derivative of ColV2-K94, was found to be incompatible with the IncFI plasmids KLF1 and R386. It was compatible with the IncFII plasmids R538 and R100. Three overlapping mini-ColV derivatives, pWS15, pWS16 and pWS17, were obtained by restriction digestion of pWS12. Unlike pWS12, pWS16 exhibited incompatibility with
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4. DnaA protein is not essential for replication of IncFII plasmid NR1.
By transformation of dnaA null mutant host cells that are suppressed either by an rnh mutation or by chromosomal integration of a mini-R1 plasmid, it was shown that replication of miniplasmids composed of the NR1 minimal replicon had no absolute dependence upon DnaA protein. In addition, the suppression of the dnaA null mutation by the integrated mini-R1, wh
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5. Microcin B17, a novel tool for preparation of maxicells: identification of polypeptides encoded by the IncFII minireplicon pMccB17.
The DNA replication inhibitor peptide microcin B17 is shown to be a useful tool for preparing Escherichia coli maxicells. To illustrate its usefulness, we have identified polypeptides synthesized from pMccB17 and R100 IncFII miniplasmids. After comparing the respective polypeptides and the miniplasmid restriction maps, we concluded that these plasmids share
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6. Analysis of the individual regulatory components of the IncFII plasmid replication control system.
Replication of the IncFII plasmid NR1 is controlled by regulating the amount of synthesis of the repA1 initiator protein at both the transcriptional and translational levels. We have examined mutations which have altered each of these levels of regulation, resulting in different plasmid copy numbers. The genes which encode each of the individual wild-type or
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7. Genetic and physical map of plasmid NR1: comparison with other IncFII antibiotic resistance plasmids.
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8. Control of replication of plasmid R1: the duplex between the antisense RNA, CopA, and its target, CopT, is processed specifically in vivo and in vitro by RNase III.
The replication frequency of IncFII plasmids is regulated through the availability of a rate-limiting protein, RepA. The synthesis of this protein is controlled post-transcriptionally by a small antisense RNA, CopA, which binds to the leader region of the RepA mRNA (CopT). In this communication we report studies of the IncFII plasmid R1. We show that the dup
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9. Regulation of transcription of the repA1 gene in the replication control region of IncFII plasmid NR1 by gene dosage of the repA2 transcription repressor protein.
Transcription of the repA1 gene of the IncFII plasmid NR1 is initiated at two promoters in the replication control region. Transcription from the upstream promoter is constitutive at a low level, whereas transcription from the downstream promoter is regulated. The 5' end of the constitutively synthesized transcript also encodes the transcription repressor pr
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10. Expression of the repA1 gene of IncFII plasmid NR1 is translationally coupled to expression of an overlapping leader peptide.
Examination of a group of mutants of plasmid NR1 that had lost the expression of IncFII plasmid incompatibility (Inc-) revealed a group that had also lost replication proficiency (Rep-). These mutants were obtained from plasmids in which the NR1 replication control region was present in a cointegrate with plasmid pBR322. Whereas the wild-type parental cointe
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11. Autoregulation of the stability operon of IncFII plasmid NR1.
The stb locus of IncFII plasmid NR1, which mediates stable inheritance of the plasmid, is composed of an essential cis-acting DNA site located upstream from two tandem genes that encode essential stability proteins. The two tandem genes, stbA and stbB, are transcribed as an operon from promoter PAB. Using PAB-lacZ gene fusions, it was found that the stb oper
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12. The incompatibility product of IncFII R plasmid NR1 controls gene expression in the plasmid replication region.
The incompatibility properties of IncFII R plasmid NR1 were compared with those of two of its copy number mutants, pRR12 and pRR21. pRR12 produced an altered incompatibility product and also had an altered incompatibility target site. The target site appeared to be located within the incompatibility gene, which is located more than 1,200 base pairs from the