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The role of the 3 untranslated region (3UTR) in the replication of enteroviruses has been studied with a series of mutants derived from either poliovirus type 3 (PV3) or a PV3 replicon containing the reporter gene chloramphenicol acetyltransferase. Replication was observed when the PV3 3UTR was replaced with that of either coxsackie B4 virus, human rhinovirus 14 (HRV14), bovine enterovirus, or hepatitis A virus, despite the lack of sequence and secondary structure homology of the 3UTRs of these viruses. The levels of replication observed for recombinants containing the 3UTRs of hepatitis A virus and bovine enterovirus were lower than those for PV3 and the other recombinants. Extensive site-directed mutagenesis of the single stem-loop structure formed by the HRV14 3UTR indicated the importance of (i) the loop sequence, (ii) the stability of the stem, and (iii) the location of the stem immediately upstream of the poly(A) tail. The role of a 4-bp motif at the base of the HRV14 stem, highly ...

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The functionality of a 3422-base pair promoter fragment from the mouse α1B-adrenergic receptor (α1BAR) gene was examined. This fragment, cloned from a mouse genomic library, was found to have significant sequence homology to the known human and rat α1BAR promoters. However, the consensus motif of several key cis-acting elements is not conserved among the rat, human, and mouse genes, suggesting species specificity. Confirming fidelity of the murine promoter, robust in vitro expression of a chloramphenicol acetyltransferase (CAT) reporter was detected in known α1BAR-expressing BC3H1, NB41A3, and DDT1MF-2 cells transiently transfected with a promoter-CAT construct. Conversely, minimal CAT expression was detected in known α1BAR-negative RAT-1 and R3T3 cells. These findings were extended by transfecting the same promoter-CAT construct into various primary cell types. In support of the hypothesis that α1ARs are differentially expressed in the smooth muscle of the vasculature, primary cultures of ...

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Chloramphenicol is an antibacterial aboriginal abandoned from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a almost simple anatomy and was the aboriginal broad-spectrum antibacterial to be discovered. It acts by interfering with bacterial protein amalgam and is mainly bacteriostatic. Chloramphenicol is an Amphenicol-class Antibacterial. The actinic allocation of chloramphenicol is…

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Group B chloramphenicol acetyltransferase, which can inactivate chloramphenicol. Also referred to as xenobiotic acetyltransferase ...

Leuconostoc에서 자가복제되는 셔틀벡터를 제작하기 위해 동치미김치로부터 약 200종의 Leuconostoc 예상균주를 분리하였고 이들 중 8 종의 균주에서 10 kb 이하의 플라스미드 DNA를 확인하였다. 이들 플라스미드들은 southern hybridization에 의하여 두 가지의 상동그룹, 즉 pCB18 상동그룹과 pCB42 상동그룹으로 분류할 수 있었다. 위 두개의 플라스미드를 각각 함유한 두 균주를 생화학적 분석과 16S rRNA 염기서열을 분석한 결과 Leuc. citreum으로 판명되었다. 플라스미드 pCB18은 1,821개의 염기로 이루어져 있고, 하나의 ORF를 가지며 replicase와 높은 아미노산 서열의 상동성을 보였다. 플라스미드 pCB42는 4,231개의 염기로 이루어져 있고, 두개의 ORF를 함유하고 있으며 ORF1은 transposase 단백질, ORF2는 DNA 결합 단백질과 상동성을 나타내었다. pCB18와 staphylococcal chloramphenicol acetyltransferase (CAT) ...

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TY - JOUR. T1 - Gonadotropin regulation of the rat proopiomelanocortin promoter. T2 - Characterization by transfection of primary ovarian granulosa cells. AU - Young, Steven L.. AU - Nielsen, Christian P.. AU - Lundblad, James R.. AU - Roberts, James L.. AU - Meiner, Michael H.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1989/1. Y1 - 1989/1. N2 - To characterize the transcriptional effects of human (h)FSH and hCG on the POMC gene, primary rat granulosa cells were transiently transfected with a chloramphenicol acetyltransferase (CAT) reporter plasmid under the control of the POMC promoter and 5′ region. POMC-CAT contains a fragment of the rat POMC gene, extending from nucleotide-704 to nucleotide +63, fused to the CAT gene. Treatment of POMC-CAT-transfected cells with either hFSH (20 ng/ml) or hCG (10 ng/ml) significantly increased CAT enzyme activity; however, neither hCG nor hFSH increased CAT enzyme activity in cells transfected with pSV2-CAT, a reporter plasmid ...

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klor am fen i kol). Chloramphenicol injection may cause a decrease in the number of certain types of blood cells in the body. In some cases, people who experienced this decrease in blood cells later developed leukemia (cancer that begins in the white blood cells). You may experience this decrease in blood cells whether you are being treated with chloramphenicol for a long time or a short time. If you experience any of the following symptoms, call your doctor immediately: pale skin; excessive tiredness; shortness of breath; dizziness; fast heartbeat; unusual bruising or bleeding; or signs of infection such as sore throat, fever, cough, and chills. Your doctor will order laboratory tests regularly during your treatment to check whether the number of blood cells in your body has decreased. You should know that these tests do not always detect changes in the body that may lead to a permanent decrease in the number of blood cells. It is best that you receive chloramphenicol injection in the hospital ...

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Chloramphenicol is an anti-biotic that due to its pH, it shines above most other antibiotics in terms of ability to penetrate into infected tissues and tissues with biological barriers. Unfortunately, chloramphenicol must be given typically three times daily for dogs.

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Chloramphenicol acetyltransferase (or CAT) is a bacterial enzyme (EC 2.3.1.28) that detoxifies the antibiotic chloramphenicol and is responsible for chloramphenicol resistance in bacteria. This enzyme covalently attaches an acetyl group from acetyl-CoA to chloramphenicol, which prevents chloramphenicol from binding to ribosomes. A histidine residue, located in the C-terminal section of the enzyme, plays a central role in its catalytic mechanism. The crystal structure of the type III enzyme from Escherichia coli with chloramphenicol bound has been determined. CAT is a trimer of identical subunits (monomer Mr 25,000) and the trimeric structure is stabilised by a number of hydrogen bonds, some of which result in the extension of a beta-sheet across the subunit interface. Chloramphenicol binds in a deep pocket located at the boundary between adjacent subunits of the trimer, such that the majority of residues forming the binding pocket belong to one subunit while the catalytically essential histidine ...

Plasmid-encoded fusidic acid resistance in Escherichia coli is mediated by a common variant of chloramphenicol acetyltransferase (EC 2.3.1.28), an enzyme which is an effector of chloramphenicol resistance. Resistance to chloramphenicol is a consequence of acetylation of the antibiotic catalysed by the enzyme and the failure of the 3-acetoxy product to bind to bacterial ribosomes. Cell-free coupled transcription and translation studies are in agreement with genetic studies which indicated that the entire structural gene for the type I chloramphenicol acetyltransferase is necessary for the fusidic acid resistance phenotype. The mechanism of resistance does nor involve covalent modification of the antibiotic. The other naturally-occurring enterobacterial chloramphenicol acetyltransferase variants (types II and III) do not cause fusidic acid resistance. Steady-state kinetic studies with the type I enzyme have shown that the binding of fusidic acid is competitive with respect to chloramphenicol. The ...

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