Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nucleotide sequence of the chloramphenicol acetyltransferase gene (cat) and its regulatory region, encoded by the plasmid pSCS7 from Staphylococcus aureus, was determined. The structural cat gene encoded a protein of 209 amino acids, which represented one monomer of the enzyme chloramphenicol acetyltransferase (CAT). Comparisons between the amino acid sequences of the pSCS7-encoded CAT from S. aureus and the previously sequenced CAT variants from S. aureus, Staphylococcus intermedius, Staphylococcus haemolyticus, Bacillus pumilis, Clostridium difficile, Clostridium perfringens, Escherichia coli, Shigella flexneri, and Proteus mirabilis were performed. An alignment of CAT amino acid sequences demonstrated the presence of 34 conserved amino acids among all CAT variants. These conserved residues were considered for their possible roles in the structure and function of CAT. On the basis of the alignment, a phylogenetic tree was constructed. It demonstrated relatively large evolutionary distances between the CAT variants of enteric bacteria, Clostridium, Bacillus, and Staphylococcus species.
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PMID:Nucleotide sequence and phylogeny of a chloramphenicol acetyltransferase encoded by the plasmid pSCS7 from Staphylococcus aureus. 192 26

VirB plays a central role in the regulation of virulence of Shigella flexneri. It acts as a transcriptional activator and is itself transcriptionally activated by another virulence protein, VirF. Experiments were performed in order to identify the site upstream of virB at which VirF binds in order to activate transcription. Progressive 5' deletions of the DNA upstream of the transcription start point of virB were constructed by subcloning and Bal31 deletion. These deletion derivatives were cloned into the chloramphenicol acetyltransferase (CAT) reporter gene plasmid pKK232-8 and the resulting plasmids were analysed using a CAT activity assay. This allowed identification of minimal regions required for VirB promoter activity and regions required for full enhancement of promoter activity by VirF. A region approximately 100 bp upstream from the transcription start point of virB was identified as being necessary for full activation of this promoter by VirF. This region encompasses at least one inverted repeat which may play a role in transcription repression in the absence of the activator protein, VirF.
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PMID:Site of transcriptional activation of virB on the large plasmid of Shigella flexneri 2a by VirF, a member of the AraC family of transcriptional activators. 841 20

Eighty-six strains of Shigella spp. were isolated during the dry season from stool samples of children under 5 years of age in Ifakara, Tanzania. The epidemiological relationship as well as the antimicrobial susceptibility and mechanisms of resistance to ampicillin, chloramphenicol, and co-trimoxazole were investigated. Four different epidemiological tools, pulsed-field gel electrophoresis (PFGE), repetitive extragenic palindromic (REP)-PCR, plasmid analysis, and antibiogram, were compared for typing Shigella strains. Seventy-eight (90%) strains were Shigella flexneri and were distributed into four groups, by either PFGE or REP-PCR, with 51, 17, 7, and 3 strains. The four strains of Shigella dysenteriae belonged to the same group, and the four strains of Shigella sonnei were distributed in two groups with three and one strain each. Plasmid analysis showed a high level of heterogeneity among strains belonging to the same PFGE group, while the antibiogram was less discriminative. REP-PCR provided an alternative, rapid, powerful genotyping method for Shigella spp. Overall, antimicrobial susceptibility testing showed a high level of resistance to ampicillin (81.8%), chloramphenicol (72.7%), tetracycline (96.9%), and co-trimoxazole (87.9%). Ampicillin resistance was related to an integron-borne OXA-1-type beta-lactamase in 85.1% of the cases and to a TEM-1-type beta-lactamase in the remaining 14.8%. Resistance to co-trimoxazole was due to the presence of a dhfr Ia gene in all groups except one of S. flexneri, where a dhfr VII gene was found within an integron. Chloramphenicol resistance was associated in every case with positive chloramphenicol acetyltransferase activity. All strains were susceptible to nalidixic acid, ciprofloxacin, ceftazidime, cefotaxime, and cefoxitin. Therefore, these antimicrobial agents may be good alternatives for the treatment of diarrhea caused by Shigella in Tanzania.
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PMID:Typing and characterization of mechanisms of resistance of Shigella spp. isolated from feces of children under 5 years of age from Ifakara, Tanzania. 1048 63

Eighty isolates of Shigella spp. (37 Shigella flexneri and 43 Shigella sonnei) from patients with travellers' diarrhoea were studied. Susceptibility tests revealed high levels of resistance, especially to ampicillin (65%), tetracycline (78%) and trimethoprim (75%), and particularly among the S. flexneri isolates. Dihydrofolate reductase 1 genes (dfrA1) were prevalent among the trimethoprim-resistant isolates, while oxa genes predominated among the ampicillin-resistant isolates. Chloramphenicol resistance was associated with production of chloramphenicol acetyltransferase, while nalidixic acid-resistant isolates had a single mutation in the gyrA gene. The results indicate a continuing need for resistance surveillance and rational use of antimicrobial agents.
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PMID:Analysis of the mechanisms of resistance to several antimicrobial agents in Shigella spp. causing travellers' diarrhoea. 1630 63