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Journal articles on the topic 'Fazi AHP'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Anisseh, Mohammad, Fatemeh Hemmati, and Reza Shahraki. "Best selection of project portfolio using Fuzzy AHP and Fuzzy TOPSIS." Journal of Engineering Management and Competitiveness 8, no. 1 (2018): 3–10. http://dx.doi.org/10.5937/jemc1801003a.

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2

Petrović, Ivan, Miodrag Gordić, and Milan Kankaraš. "Fazi: AHP pristup u vrednovanju kriterijuma za izbor raketnog sistema za protivvazduhoplovna dejstva." Vojno delo 70, no. 4 (2018): 298–308. http://dx.doi.org/10.5937/vojdelo1802298p.

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3

Hoang, Tung T., and Herbert P. Schweizer. "Characterization of Pseudomonas aeruginosa Enoyl-Acyl Carrier Protein Reductase (FabI): a Target for the Antimicrobial Triclosan and Its Role in Acylated Homoserine Lactone Synthesis." Journal of Bacteriology 181, no. 17 (September 1, 1999): 5489–97. http://dx.doi.org/10.1128/jb.181.17.5489-5497.1999.

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ABSTRACT The Pseudomonas aeruginosa fabI structural gene, encoding enoyl-acyl carrier protein (ACP) reductase, was cloned and sequenced. Nucleotide sequence analysis revealed that fabIis probably the last gene in a transcriptional unit that includes a gene encoding an ATP-binding protein of an ABC transporter of unknown function. The FabI protein was similar in size and primary sequence to other bacterial enoyl-ACP reductases, and it contained signature motifs for the FAD-dependent pyridine nucleotide reductase and glucose/ribitol dehydrogenase families, respectively. The chromosomal fabIgene was disrupted, and the resulting mutant was viable but possessed only 62% of the total enoyl-ACP reductase activity found in wild-type cell extracts. The fabI-encoded enoyl-ACP reductase activity was NADH dependent and inhibited by triclosan; the residual activity in the fabI mutant was also NADH dependent but not inhibited by triclosan. An polyhistidine-tagged FabI protein was purified and characterized. Purified FabI (i) could use NADH but not NADPH as a cofactor; (ii) used both crotonyl-coenzyme A and crotonyl-ACP as substrates, although it was sixfold more active with crotonyl-ACP; and (iii) was efficiently inhibited by low concentrations of triclosan. A FabI Gly95-to-Val active-site amino acid substitution was generated by site-directed mutagenesis, and the mutant protein was purified. The mutant FabI protein retained normal enoyl-ACP reductase activity but was highly triclosan resistant. When coupled to FabI, purified P. aeruginosa N-butyryl-l-homoserine lactone (C4-HSL) synthase, RhlI, could synthesize C4-HSL from crotonyl-ACP and S-adenosylmethionine. This reaction was NADH dependent and inhibited by triclosan. The levels of C4-HSL andN-(3-oxo)-dodecanoyl-l-homoserine lactones were reduced 50% in a fabI mutant, corroborating the role of FabI in acylated homoserine lactone synthesis in vivo.

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Massengo-Tiassé, R. Prisca, and John E. Cronan. "Vibrio cholerae FabV Defines a New Class of Enoyl-Acyl Carrier Protein Reductase." Journal of Biological Chemistry 283, no. 3 (November 21, 2007): 1308–16. http://dx.doi.org/10.1074/jbc.m708171200.

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Enoyl-acyl carrier protein (ACP) reductase catalyzes the last step of the fatty acid elongation cycle. The paradigm enoyl-ACP reductase is the FabI protein of Escherichia coli that is the target of the antibacterial compound, triclosan. However, some Gram-positive bacteria are naturally resistant to triclosan due to the presence of the triclosan-resistant enoyl-ACP reductase isoforms, FabK and FabL. The genome of the Gram-negative bacterium, Vibrio cholerae lacks a gene encoding a homologue of any of the three known enoyl-ACP reductase isozymes suggesting that this organism encodes a novel fourth enoyl-ACP reductase isoform. We report that this is the case. The gene encoding the new isoform, called FabV, was isolated by complementation of a conditionally lethal E. coli fabI mutant strain and was shown to restore fatty acid synthesis to the mutant strain both in vivo and in vitro. Like FabI and FabL, FabV is a member of the short chain dehydrogenase reductase superfamily, although it is considerably larger (402 residues) than either FabI (262 residues) or FabL (250 residues). The FabV, FabI and FabL sequences can be aligned, but only poorly. Alignment requires many gaps and yields only 15% identical residues. Thus, FabV defines a new class of enoyl-ACP reductase. The native FabV protein has been purified to homogeneity and is active with both crotonyl-ACP and the model substrate, crotonyl-CoA. In contrast to FabI and FabL, FabV shows a very strong preference for NADH over NADPH. Expression of FabV in E. coli results in markedly increased resistance to triclosan and the purified enzyme is much more resistant to triclosan than is E. coli FabI.

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Zhu, Lei, Jinshui Lin, Jincheng Ma, John E. Cronan, and Haihong Wang. "Triclosan Resistance of Pseudomonas aeruginosa PAO1 Is Due to FabV, a Triclosan-Resistant Enoyl-Acyl Carrier Protein Reductase." Antimicrobial Agents and Chemotherapy 54, no. 2 (November 23, 2009): 689–98. http://dx.doi.org/10.1128/aac.01152-09.

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ABSTRACT Triclosan, a very widely used biocide, specifically inhibits fatty acid synthesis by inhibition of enoyl-acyl carrier protein (ACP) reductase. Escherichia coli FabI is the prototypical triclosan-sensitive enoyl-ACP reductase, and E. coli is extremely sensitive to the biocide. However, other bacteria are resistant to triclosan, because they encode triclosan-resistant enoyl-ACP reductase isozymes. In contrast, the triclosan resistance of Pseudomonas aeruginosa PAO1 has been attributed to active efflux of the compound (R. Chuanchuen, R. R. Karkhoff-Schweizer, and H. P. Schweizer, Am. J. Infect. Control 31:124-127, 2003). We report that P. aeruginosa contains two enoyl-ACP reductase isozymes, the previously characterized FabI homologue plus a homologue of FabV, a triclosan-resistant enoyl-ACP reductase recently demonstrated in Vibrio cholerae. By deletion of the genes encoding P. aeruginosa FabI and FabV, we demonstrated that FabV confers triclosan resistance on P. aeruginosa. Upon deletion of the fabV gene, the mutant strain became extremely sensitive to triclosan (>2,000-fold more sensitive than the wild-type strain), whereas the mutant strain lacking FabI remained completely resistant to the biocide.

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6

Demissie, Robel D., Pauline Kabre, Micheal L. Tuntland, and Leslie W. M. Fung. "An Efficient and Economical Assay to Screen for Triclosan Binding to FabI." Journal of Biomolecular Screening 21, no. 4 (November 4, 2015): 391–98. http://dx.doi.org/10.1177/1087057115615085.

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Triclosan is an effective inhibitor for enoyl acyl carrier protein reductase (ENR) in fatty acid biosynthesis. Triclosan-resistant mutants of ENR have emerged. Thus, it is important to detect these triclosan-resistant mutations in ENR. Generally, enzyme activity assays on the mutants are used to determine the effect of triclosan on ENR activity. Since the substrates are linked to acyl carrier protein (ACP), the assays are challenging due to the need to prepare the ACP and link it to the substrates. Non-ACP-linked (coenzyme A [CoA]-linked) substrates can be used in some ENR, but not in all. Consequently, screening for triclosan-resistant mutants is also challenging. We have developed a simple thermal shift assay, which does not use ACP-linked substrates, to determine the binding ability of triclosan to the ENR active site, and thus it can be used for screening for triclosan-resistant mutants. Staphylococcus aureus FabI enzyme and its mutants were used to demonstrate the binding ability of triclosan with NADP+ to FabI. The direct correlation between the binding ability and enzyme activity was demonstrated with Francisella tularensis FabI. This method may also be applied to select effective triclosan analogues that inhibit ENR activity.

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7

Payne, David J., William H. Miller, Valerie Berry, John Brosky, Walter J. Burgess, Emile Chen, Walter E. DeWolf, et al. "Discovery of a Novel and Potent Class of FabI-Directed Antibacterial Agents." Antimicrobial Agents and Chemotherapy 46, no. 10 (October 2002): 3118–24. http://dx.doi.org/10.1128/aac.46.10.3118-3124.2002.

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ABSTRACT Bacterial enoyl-acyl carrier protein (ACP) reductase (FabI) catalyzes the final step in each elongation cycle of bacterial fatty acid biosynthesis and is an attractive target for the development of new antibacterial agents. High-throughput screening of the Staphylococcus aureus FabI enzyme identified a novel, weak inhibitor with no detectable antibacterial activity against S. aureus. Iterative medicinal chemistry and X-ray crystal structure-based design led to the identification of compound 4 [(E)-N-methyl-N-(2-methyl-1H-indol-3-ylmethyl)-3-(7-oxo-5,6,7,8-tetrahydro-1,8-naphthyridin-3-yl)acrylamide], which is 350-fold more potent than the original lead compound obtained by high-throughput screening in the FabI inhibition assay. Compound 4 has exquisite antistaphylococci activity, achieving MICs at which 90% of isolates are inhibited more than 500 times lower than those of nine currently available antibiotics against a panel of multidrug-resistant strains of S. aureus and Staphylococcus epidermidis. Furthermore, compound 4 exhibits excellent in vivo efficacy in an S. aureus infection model in rats. Biochemical and genetic approaches have confirmed that the mode of antibacterial action of compound 4 and related compounds is via inhibition of FabI. Compound 4 also exhibits weak FabK inhibitory activity, which may explain its antibacterial activity against Streptococcus pneumoniae and Enterococcus faecalis, which depend on FabK and both FabK and FabI, respectively, for their enoyl-ACP reductase function. These results show that compound 4 is representative of a new, totally synthetic series of antibacterial agents that has the potential to provide novel alternatives for the treatment of S. aureus infections that are resistant to our present armory of antibiotics.

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Schaeffer, Merrill L., Gautam Agnihotri, Craig Volker, Howard Kallender, Patrick J. Brennan, and John T. Lonsdale. "Purification and Biochemical Characterization of theMycobacterium tuberculosisβ-Ketoacyl-acyl Carrier Protein Synthases KasA and KasB." Journal of Biological Chemistry 276, no. 50 (October 12, 2001): 47029–37. http://dx.doi.org/10.1074/jbc.m108903200.

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Mycolic acids are vital components of theMycobacterium tuberculosiscell wall, and enzymes involved in their formation represent attractive targets for the discovery of novel anti-tuberculosis agents. Biosynthesis of the fatty acyl chains of mycolic acids involves two fatty acid synthetic systems, the multifunctional polypeptide fatty acid synthase I (FASI), which performsde novofatty acid synthesis, and the dissociated FASII system, which consists of monofunctional enzymes, and acyl carrier protein (ACP) and elongates FASI products to long chain mycolic acid precursors. In this study, we present the initial characterization of purified KasA and KasB, two β-ketoacyl-ACP synthase (KAS) enzymes of theM. tuberculosisFASII system. KasA and KasB were expressed inE. coliand purified by affinity chromatography. Both enzymes showed activity typical of bacterial KASs, condensing an acyl-ACP with malonyl-ACP. Consistent with the proposed role of FASII in mycolic acid synthesis, analysis of various acyl-ACP substrates indicated KasA and KasB had higher specificity for long chain acyl-ACPs containing at least 16 carbons. Activity of KasA and KasB increased with use ofM. tuberculosisAcpM, suggesting that structural differences between AcpM andE. coliACP may affect their recognition by the enzymes. Both enzymes were sensitive to KAS inhibitors cerulenin and thiolactomycin. These results represent important steps in characterizing KasA and KasB as targets for antimycobacterial drug discovery.

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9

Fan, Frank, Kang Yan, Nicola G. Wallis, Shannon Reed, Terrance D. Moore, Stephen F. Rittenhouse, Walter E. DeWolf, et al. "Defining and Combating the Mechanisms of Triclosan Resistance in Clinical Isolates of Staphylococcus aureus." Antimicrobial Agents and Chemotherapy 46, no. 11 (November 2002): 3343–47. http://dx.doi.org/10.1128/aac.46.11.3343-3347.2002.

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ABSTRACT The MICs of triclosan for 31 clinical isolates of Staphylococcus aureus were 0.016 μg/ml (24 strains), 1 to 2 μg/ml (6 strains), and 0.25 μg/ml (1 strain). All the strains for which triclosan MICs were elevated (>0.016 μg/ml) showed three- to fivefold increases in their levels of enoyl-acyl carrier protein (ACP) reductase (FabI) production. Furthermore, strains for which triclosan MICs were 1 to 2 μg/ml overexpressed FabI with an F204C alteration. Binding studies with radiolabeled NAD+ demonstrated that this change prevents the formation of the stable triclosan-NAD+-FabI complex, and both this alteration and its overexpression contributed to achieving MICs of 1 to 2 μg/ml for these strains. Three novel, potent inhibitors of FabI (50% inhibitory concentrations, ≤64 nM) demonstrated up to 1,000-fold better activity than triclosan against the strains for which triclosan MICs were elevated. None of the compounds tested from this series formed a stable complex with NAD+-FabI. Consequently, although the overexpression of wild-type FabI gave rise to an increase in the MICs, as expected, overexpression of FabI with an F204C alteration did not cause an additional increase in resistance. Therefore, this work identifies the mechanisms of triclosan resistance in S. aureus, and we present three compounds from a novel chemical series of FabI inhibitors which have excellent activities against both triclosan-resistant and -sensitive clinical isolates of S. aureus.

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10

Stölzel, Ulrich, and Detlef Schuppan. "Neue Therapieoption für akute hepatische Porphyrien." DMW - Deutsche Medizinische Wochenschrift 146, no. 15 (August 2021): 955–58. http://dx.doi.org/10.1055/a-1282-1156.

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Was ist neu? Therapie mit Givosiran Givosiran ist ein kleines synthetisches doppelsträngiges siRNA-Fragment mit 20 Basenpaaren Länge. Eine prospektive, randomisierte multizentrische Studie (Envision) zeigte erstmalig die klinische Wirksamkeit von monatlich subkutan applizierten synthetischen RNA-Molekülen („small interfering“ RNA, siRNA) zur Prävention von Attacken bei akuten hepatischen Porphyrien (AHP) 2. Die Koppelung von siRNA-Molekülen an N-Acetyl-Galaktosamin (GalNAc) und die hierdurch leberspezifische Aufnahme durch den Asialoglykoprotein-Rezeptor auf Hepatozyten sind ein Meilenstein in der Hepatologie. Dies führt zu einer hochselektiven Inhibition der Translation der bei AHP überexprimierten hepatischen Aminolävulinsäure-Synthase (ALAS1). Givosiran wurde in den USA und in Europa zur Behandlung akuter hepatischer Porphyrien zugelassen. Fazit Der Erfolg dieser innovativen Therapie eröffnet die Möglichkeit, prinzipiell jeden Prozess auf der Ebene der hepatozytären mRNA-Translation zu hemmen. Der therapeutische Effekt der stabilisierten siRNA hält über Wochen an. Die Behandlung mit Givosiran ist aktuell jedoch sehr kostenintensiv. Aufgrund von bislang unverstandenen Veränderungen der Nierenfunktion und Aminotransferasen ist im ersten halben Jahr zudem eine monatliche Überwachung nötig.

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11

Miller, William H., Mark A. Seefeld, Kenneth A. Newlander, Irene N. Uzinskas, Walter J. Burgess, Dirk A. Heerding, Catherine C. K. Yuan, et al. "Discovery of Aminopyridine-Based Inhibitors of Bacterial Enoyl-ACP Reductase (FabI)." Journal of Medicinal Chemistry 45, no. 15 (July 2002): 3246–56. http://dx.doi.org/10.1021/jm020050+.

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12

Cioch, Maria. "Ruksolitynib w leczeniu pierwotnej mielofibrozy w fazie akceleracji i z małopłytkowością – opis przypadku." Acta Haematologica Polonica 49, no. 3 (December 31, 2018): 147–50. http://dx.doi.org/10.2478/ahp-2018-0022.

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StreszczeniePierwotna mielofibroza (primary myelofibrosis – PMF) jest Ph-negatywnym nowotworem mieloproliferacyjnym, charakteryzującym się włóknieniem szpiku, cytopeniami oraz objawami ogólnymi, które w istotny sposób wpływają na jakość i długość życia. Stosowanie ruksolitynibu, inhibitora kinaz JAK1 i JAK2 prowadzi do zmniejszenia wymiarów śledziony, a także nasilenia objawów ogólnych, co poprawia jakość życia. Tego typu terapia rekomendowana jest u chorych z objawową mielofibrozą z grupy ryzyka pośredniego 2 i wysokiego. Opublikowano dotąd niewiele doniesień dotyczących zastosowania ruksolitynibu w zaawansowanych fazach PMF: akceleracji i zaostrzenia blastycznego. Ważnym klinicznie problemem jest także prowadzenie chorych ze współistniejącą małopłytkowością.W pracy przedstawiono chorą na PMF, u której ruksolitynib z dobrym skutkiem stosowany jest od 4 lat w fazie akceleracji, przy współistniejącej małopłytkowości. Rozpoznanie PMF postawiono w 2008 r. W ciągu piewszych 5 lat w leczeniu stosowano hydroksykarbamid, talidomid, prednizon i radioterapię śledziony. W roku 2013 rozpoznano akcelerację choroby, charakteryzującą się obecnością 10% blastów w szpiku, splenomegalią dużego stopnia, małopłytkowością oraz nasileniem objawów ogólnych. Leczenie ruksolitynibem rozpoczęto w grudniu 2013 r. Dawka leku, zależnie od liczby płytek krwi, wahała sie od 5 mg raz dziennie do 20 mg 2 razy dziennie. Terapia ruksolitynibem jest kontynuowana do dzisiaj, tj. ponad 4 lata. Jej efektem jest redukcja wymiarów śledziony, ustąpienie objawów ogólnych, poprawa jakości życia oraz stabilizacja odsetka komórek blastycznych w szpiku. Prezentowany przypadek jest przykładem na skuteczność ruksolitynibu w fazie zaawansowanej PMF dzięki indywidualizacji dawkowania leku.

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13

Kingry, Luke C., Jason E. Cummings, Kerry W. Brookman, Gopal R. Bommineni, Peter J. Tonge, and Richard A. Slayden. "The Francisella tularensis FabI Enoyl-Acyl Carrier Protein Reductase Gene Is Essential to Bacterial Viability and Is Expressed during Infection." Journal of Bacteriology 195, no. 2 (November 9, 2012): 351–58. http://dx.doi.org/10.1128/jb.01957-12.

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ABSTRACTFrancisella tularensisis classified as a category A priority pathogen and causes fatal disseminated disease in humans upon inhalation of less than 50 bacteria. Although drugs are available for treatment, they are not ideal because of toxicity and route of delivery, and in some cases patients relapse upon withdrawal. We have an ongoing program to develop novel FAS-II FabI enoyl-ACP reductase enzyme inhibitors forFrancisellaand other select agents. To establishF. tularensisFabI (FtFabI) as a clinically relevant drug target, we demonstrated that fatty acid biosynthesis and FabI activity are essential for growth even in the presence of exogenous long-chain lipids and that FtfabIis not transcriptionally altered in the presence of exogenous long-chain lipids. Inhibition of FtFabI or fatty acid synthesis results in loss of viability that is not rescued by exogenous long-chain lipid supplementation. Importantly, whole-genome transcriptional profiling ofF. tularensiswith DNA microarrays from infected tissues revealed that FtfabIandde novofatty acid biosynthetic genes are transcriptionally active during infection. This is the first demonstration that the FabI enoyl-ACP-reductase enzyme encoded byF. tularensisis essential and not bypassed by exogenous fatty acids and thatde novofatty acid biosynthetic components encoded inF. tularensisare transcriptionally active during infection in the mouse model of tularemia.

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MARRAKCHI, Hedia, Walter E. DeWOLF, Chad QUINN, Joshua WEST, Brian J. POLIZZI, Chi Y. SO, David J. HOLMES, et al. "Characterization of Streptococcus pneumoniae enoyl-(acyl-carrier protein) reductase (FabK)." Biochemical Journal 370, no. 3 (March 15, 2003): 1055–62. http://dx.doi.org/10.1042/bj20021699.

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The enoyl-(acyl-carrier protein) (ACP) reductase catalyses the last step in each cycle of fatty acid elongation in the type II fatty acid synthase systems. An extensively characterized NADH-dependent reductase, FabI, is widely distributed in bacteria and plants, whereas the enoyl-ACP reductase, FabK, is a distinctly different member of this enzyme group discovered in Streptococcus pneumoniae. We were unable to delete the fabK gene from Strep. pneumoniae, suggesting that this is the only enoyl-ACP reductase in this organism. The FabK enzyme was purified and the biochemical properties of the reductase were examined. The visible absorption spectrum of the purified protein indicated the presence of a flavin cofactor that was identified as FMN by MS, and was present in a 1:1 molar ratio with protein. FabK specifically required NADH and the protein activity was stimulated by ammonium ions. FabK also exhibited NADH oxidase activity in the absence of substrate. Strep. pneumoniae belongs to the Bacillus/Lactobacillus/Streptococcus group that includes Staphylococcus aureus and Bacillus subtilis. These two organisms also contain FabK-related genes, suggesting that they may also express a FabK-like enoyl-ACP reductase. However, the genes did not complement a fabI(Ts) mutant and the purified flavoproteins were unable to reduce enoyl-ACP in vitro and did not exhibit NAD(P)H oxidase activity, indicating they were not enoyl-ACP reductases. The restricted occurrence of the FabK enoyl-ACP reductase may be related to the role of substrate-independent NADH oxidation in oxygen-dependent anaerobic energy metabolism.

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KAPOOR, Mili, C. Chandramouli REDDY, M. V. KRISHNASASTRY, Namita SUROLIA, and Avadhesha SUROLIA. "Slow-tight-binding inhibition of enoyl-acyl carrier protein reductase from Plasmodium falciparum by triclosan." Biochemical Journal 381, no. 3 (July 27, 2004): 719–24. http://dx.doi.org/10.1042/bj20031821.

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Triclosan is a potent inhibitor of FabI (enoyl-ACP reductase, where ACP stands for acyl carrier protein), which catalyses the last step in a sequence of four reactions that is repeated many times with each elongation step in the type II fatty acid biosynthesis pathway. The malarial parasite Plasmodium falciparum also harbours the genes and is capable of synthesizing fatty acids by utilizing the enzymes of type II FAS (fatty acid synthase). The basic differences in the enzymes of type I FAS, present in humans, and type II FAS, present in Plasmodium, make the enzymes of this pathway a good target for antimalarials. The steady-state kinetics revealed time-dependent inhibition of FabI by triclosan, demonstrating that triclosan is a slow-tight-binding inhibitor of FabI. The inhibition followed a rapid equilibrium step to form a reversible enzyme–inhibitor complex (EI) that isomerizes to a second enzyme–inhibitor complex (EI*), which dissociates at a very slow rate. The rate constants for the isomerization of EI to EI* and the dissociation of EI* were 5.49×10−2 and 1×10−4 s−1 respectively. The Ki value for the formation of the EI complex was 53 nM and the overall inhibition constant Ki* was 96 pM. The results match well with the rate constants derived independently from fluorescence analysis of the interaction of FabI and triclosan, as well as those obtained by surface plasmon resonance studies [Kapoor, Mukhi, N. Surolia, Sugunda and A. Surolia (2004) Biochem. J. 381, 725–733].

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Aulawi, Hilmi, and Ridwan Jauhari. "Analisis Keputusan Pembelian Mesin Rajut Otomatis dengan Menggunakan Metode AHP dan SAW." Jurnal Kalibrasi 18, no. 2 (February 27, 2021): 66–71. http://dx.doi.org/10.33364/kalibrasi/v.18-2.733.

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Tujuan penelitian ini yaitu untuk mengetahui alternatif terbaik dalam pembelian mesin rajut otomatis berbasis komputer dan mengetahui kriteria-kriteria yang harus dipertimbangkan mesin tersebut, sehingga dapat digunakan untuk menyelesaikan permasalahan di PD Fauzi Perdana Abadi yaitu terjadinya turnover karyawan yang sangat berpengaruh terhadap proses produksi yang dilakukan. Pemecahan masalah ini menggunakan dua pendekatan dalam sistem pendukung keputusan antara lain Metode Analytical Hierarchy Process dan Simple Additive Wieghting, dengan metode AHP sendiri memiliki kelebihan yaitu dapat mengakomodir pendapat-pendapat dari stakeholder, akan tetapi dari sisi lain mesin rajut otomatis sendiri memiliki spesifikasi teknis dari mesin – mesin yang ditawarkan tersedia, alangkah lebih baik jika pada proses pemilihanya melibatkan model pengabilan keputusan yang berbasis kuantitatif, model pengambilan keputusan yang relevan untuk digunakan yaitu adalah SAW. Hasil yang didapat bahwa urutan faktor-faktor pendukung untuk pembelian mesin rajut otomatis ini berdasarkan bobot terbesar hingga terkecil adalah harga, biaya perawatan, kapasitas produksi, daya listrik dan usia pakai. Kemudian dari lima alternatif mesin rajut otomatis yang dapat dibeli, berdasarkan hasil perhitungan menggunakan SAW dengan perolehan bobot terbesar adalah alternatif ke 5 (A5).

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Liu, N., J. E. Cummings, K. England, R. A. Slayden, and P. J. Tonge. "Mechanism and inhibition of the FabI enoyl-ACP reductase from Burkholderia pseudomallei." Journal of Antimicrobial Chemotherapy 66, no. 3 (January 22, 2011): 564–73. http://dx.doi.org/10.1093/jac/dkq509.

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Seefeld, Mark A., William H. Miller, Kenneth A. Newlander, Walter J. Burgess, Walter E. DeWolf, Patricia A. Elkins, Martha S. Head, et al. "Indole Naphthyridinones as Inhibitors of Bacterial Enoyl-ACP Reductases FabI and FabK." Journal of Medicinal Chemistry 46, no. 9 (April 2003): 1627–35. http://dx.doi.org/10.1021/jm0204035.

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Kitagawa, Hideo, Ko Kumura, Sho Takahata, Maiko Iida, and Kunio Atsumi. "4-Pyridone derivatives as new inhibitors of bacterial enoyl-ACP reductase FabI." Bioorganic & Medicinal Chemistry 15, no. 2 (January 2007): 1106–16. http://dx.doi.org/10.1016/j.bmc.2006.10.012.

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20

Bergler, H., P. Wallner, A. Ebeling, B. Leitinger, S. Fuchsbichler, H. Aschauer, G. Kollenz, G. Högenauer, and F. Turnowsky. "Protein EnvM is the NADH-dependent enoyl-ACP reductase (FabI) of Escherichia coli." Journal of Biological Chemistry 269, no. 8 (February 1994): 5493–96. http://dx.doi.org/10.1016/s0021-9258(17)37485-9.

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Asse Junior, Leonardo Rander, Thales Kronenberger, Mateus Sá Magalhães Serafim, Yamara Viana Sousa, Isabella Drumond Franco, Marilia Valli, Vanderlan da Silva Bolzani, et al. "Virtual screening of antibacterial compounds by similarity search of Enoyl-ACP reductase (FabI) inhibitors." Future Medicinal Chemistry 12, no. 1 (January 2020): 51–68. http://dx.doi.org/10.4155/fmc-2019-0158.

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Aim: Antibiotic resistance is an alarming issue, as multidrug-resistant bacteria are growing worldwide, hence the decrease of therapeutic potential of available antibiotic arsenal. Among these bacteria, Staphylococcus aureus was pointed by the WHO in the pathogens list to be prioritized in drug development. Methods: We report the use of chemical similarity models for the virtual screening of new antibacterial with structural similarity to known inhibitors of FabI. The potential inhibitors were experimentally evaluated for antibacterial activity and membrane disrupting capabilities. Results & conclusion: These models led to the finding of four new compounds with antibacterial activity, one of which having antimicrobial activity already reported in the literature.

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Takhi, Mohamed, Kandepu Sreenivas, Chandrashekar K. Reddy, Mahadari Munikumar, Kolakota Praveena, Pabolu Sudheer, Bandaru N. V. M. Rao, et al. "Discovery of azetidine based ene-amides as potent bacterial enoyl ACP reductase (FabI) inhibitors." European Journal of Medicinal Chemistry 84 (September 2014): 382–94. http://dx.doi.org/10.1016/j.ejmech.2014.07.036.

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Kim, Kook-Han, Byung Hak Ha, Su Jin Kim, Seung Kon Hong, Kwang Yeon Hwang, and Eunice EunKyeong Kim. "Crystal Structures of Enoyl-ACP Reductases I (FabI) and III (FabL) from B. subtilis." Journal of Molecular Biology 406, no. 3 (February 2011): 403–15. http://dx.doi.org/10.1016/j.jmb.2010.12.003.

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Yao, Jingjing, Qingye Zhang, Jun Min, Jin He, and Ziniu Yu. "Novel enoyl-ACP reductase (FabI) potential inhibitors of Escherichia coli from Chinese medicine monomers." Bioorganic & Medicinal Chemistry Letters 20, no. 1 (January 2010): 56–59. http://dx.doi.org/10.1016/j.bmcl.2009.11.042.

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Yogiara, Elena A. Mordukhova, Dooil Kim, Won-Gon Kim, Jae-Kwan Hwang, and Jae-Gu Pan. "The food-grade antimicrobial xanthorrhizol targets the enoyl-ACP reductase (FabI) in Escherichia coli." Bioorganic & Medicinal Chemistry Letters 30, no. 24 (December 2020): 127651. http://dx.doi.org/10.1016/j.bmcl.2020.127651.

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Pasqualoto, Kerly F M., and Márcia M C. Ferreira. "Application of a Receptor Pruning Methodology to the Enoyl-ACP Reductase fromEscherichia coli (FabI)." QSAR & Combinatorial Science 25, no. 7 (July 2006): 629–36. http://dx.doi.org/10.1002/qsar.200530182.

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Fischer, Taylor L., Robert J. White, Katherine F. K. Mares, Devin E. Molnau, and Justin J. Donato. "ucFabV Requires Functional Reductase Activity to Confer Reduced Triclosan Susceptibility in Escherichia coli." Journal of Molecular Microbiology and Biotechnology 25, no. 6 (2015): 394–402. http://dx.doi.org/10.1159/000441640.

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<b><i>Background/Aims:</i></b> We previously identified the Triclo1 fosmid in a functional metagenomic selection for clones that increased triclosan tolerance in <i>Escherichia coli</i>. The active enzyme encoded by Triclo1 is ucFabV. Although ucFabV is homologous to FabV from other organisms, ucFabV contains substitutions at key positions that would predict differences in substrate binding. Therefore, a detailed characterization of ucFabV was conducted to link its biochemical activity to its ability to confer reduced triclosan sensitivity. <b><i>Methods:</i></b> ucFabV and a catalytic mutant were purified and used to reduce crotonoyl-CoA in vitro. The mutant and wild-type enzymes were introduced into <i>E. coli</i>, and their ability to confer triclosan tolerance as well as suppress a temperature-sensitive mutant of FabI were measured. <b><i>Results:</i></b> Purified ucFabV, but not the mutant, reduced crotonoyl-CoA in vitro. The wild-type enzyme confers increased triclosan tolerance when introduced into <i>E. coli</i>, whereas the mutant remained susceptible to triclosan<i>. </i>Additionally, wild-type ucFabV, but not the mutant, functionally replaced FabI within living cells. <b><i>Conclusion:</i></b> ucFabV confers increased tolerance through its function as an enoyl-ACP reductase. Furthermore, ucFabV is capable of restoring viability in the presence of compromised FabI, suggesting ucFabV is likely facilitating an alternate step within fatty acid synthesis, bypassing FabI inhibition.

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Lu, Xiaoyun, Man Lv, Kun Huang, Ke Ding, and Qidong You. "Pharmacophore and Molecular Docking Guided 3D-QSAR Study of Bacterial Enoyl-ACP Reductase (FabI) Inhibitors." International Journal of Molecular Sciences 13, no. 6 (May 30, 2012): 6620–38. http://dx.doi.org/10.3390/ijms13066620.

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Karioti, Anastasia, Helen Skaltsa, Xujie Zhang, Peter J. Tonge, Remo Perozzo, Marcel Kaiser, Scott G. Franzblau, and Deniz Tasdemir. "Inhibiting enoyl-ACP reductase (FabI) across pathogenic microorganisms by linear sesquiterpene lactones from Anthemis auriculata." Phytomedicine 15, no. 12 (December 2008): 1125–29. http://dx.doi.org/10.1016/j.phymed.2008.02.018.

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Priyadarshi, Amit, Eunice EunKyeong Kim, and Kwang Yeon Hwang. "Structural insights into Staphylococcus aureus enoyl-ACP reductase (FabI), in complex with NADP and triclosan." Proteins: Structure, Function, and Bioinformatics 78, no. 2 (August 17, 2009): 480–86. http://dx.doi.org/10.1002/prot.22581.

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Sampson, Peter B., Christine Picard, Sean Handerson, Teresa E. McGrath, Megan Domagala, Andrew Leeson, Vladimir Romanov, et al. "Spiro-naphthyridinone piperidines as inhibitors of S. aureus and E. coli enoyl-ACP reductase (FabI)." Bioorganic & Medicinal Chemistry Letters 19, no. 18 (September 2009): 5355–58. http://dx.doi.org/10.1016/j.bmcl.2009.07.129.

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32

Samin, Nadav. "Laila Parsons. The Commander: Fawzi al-Qawuqji and the Fight for Arab Independence, 1914–1948." American Historical Review 123, no. 1 (February 1, 2018): 343–45. http://dx.doi.org/10.1093/ahr/123.1.343.

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Lee, Jeong Hye, Ae Kyung Park, Young Min Chi, and Seong Weon Jeong. "Crystal Structures ofPseudomonas aeruginosaEnoyl-ACP Reductase (FabI) in the Presence and Absence of NAD+and Triclosan." Bulletin of the Korean Chemical Society 36, no. 1 (January 2015): 322–26. http://dx.doi.org/10.1002/bkcs.10084.

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Vick, Jacob E., James M. Clomburg, Matthew D. Blankschien, Alexander Chou, Seohyoung Kim, and Ramon Gonzalez. "Escherichia coli Enoyl-Acyl Carrier Protein Reductase (FabI) Supports Efficient Operation of a Functional Reversal of the β-Oxidation Cycle." Applied and Environmental Microbiology 81, no. 4 (December 19, 2014): 1406–16. http://dx.doi.org/10.1128/aem.03521-14.

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ABSTRACTWe recently used a synthetic/bottom-up approach to establish the identity of the four enzymes composing an engineered functional reversal of the β-oxidation cycle for fuel and chemical production inEscherichia coli(J. M. Clomburg, J. E. Vick, M. D. Blankschien, M. Rodriguez-Moya, and R. Gonzalez, ACS Synth Biol 1:541–554, 2012,http://dx.doi.org/10.1021/sb3000782). While native enzymes that catalyze the first three steps of the pathway were identified, the identity of the native enzyme(s) acting as thetrans-enoyl coenzyme A (CoA) reductase(s) remained unknown, limiting the amount of product that could be synthesized (e.g., 0.34 g/liter butyrate) and requiring the overexpression of a foreign enzyme (theEuglena gracilistrans-enoyl-CoA reductase [EgTER]) to achieve high titers (e.g., 3.4 g/liter butyrate). Here, we examine several nativeE. colienzymes hypothesized to catalyze the reduction of enoyl-CoAs to acyl-CoAs. Our results indicate that FabI, the native enoyl-acyl carrier protein (enoyl-ACP) reductase (ENR) from type II fatty acid biosynthesis, possesses sufficient NADH-dependent TER activity to support the efficient operation of a β-oxidation reversal. Overexpression of FabI proved as effective asEgTER for the production of butyrate and longer-chain carboxylic acids. Given the essential nature offabI, we investigated whether bacterial ENRs from other families were able to complement afabIdeletion without promiscuous reduction of crotonyl-CoA. These characteristics fromBacillus subtilisFabL enabled ΔfabIcomplementation experiments that conclusively established that FabI encodes a native enoyl-CoA reductase activity that supports the β-oxidation reversal inE. coli.

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Hiltunen, J. K., F. Okubo, V. A. S. Kursu, K. J. Autio, and A. J. Kastaniotis. "Mitochondrial fatty acid synthesis and maintenance of respiratory competent mitochondria in yeast." Biochemical Society Transactions 33, no. 5 (October 26, 2005): 1162–65. http://dx.doi.org/10.1042/bst0331162.

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Mitochondrial FAS (fatty acid synthesis) of type II is a widely conserved process in eukaryotic organisms, with particular importance for respiratory competence and mitochondrial morphology maintenance in Saccharomyces cerevisiae. The recent characterization of three missing enzymes completes the pathway. Etr1p (enoyl thioester reductase) was identified via purification of the protein followed by molecular cloning. To study the link between FAS and cell respiration further, we also created a yeast strain that has FabI enoyl-ACP (acyl-carrier protein) reductase gene from Escherichia coli engineered to carry a mitochondrial targeting sequence in the genome, replacing the endogenous ETR1 gene. This strain is respiratory competent, but unlike the ETR1 wild-type strain, it is sensitive to triclosan on media containing only non-fermentable carbon source. A colony-colour-sectoring screen was applied for cloning of YHR067w/RMD12, the gene encoding mitochondrial 3-hydroxyacyl-ACP dehydratase (Htd2/Yhr067p), the last missing component of the mitochondrial FAS. Finally, Hfa1p was shown to be the mitochondrial acetyl-CoA carboxylase.

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Marcinkeviciene, Jovita, Wenjun Jiang, Lisa M. Kopcho, Gregory Locke, Ying Luo, and Robert A. Copeland. "Enoyl-ACP Reductase (FabI) of Haemophilus influenzae: Steady-State Kinetic Mechanism and Inhibition by Triclosan and Hexachlorophene." Archives of Biochemistry and Biophysics 390, no. 1 (June 2001): 101–8. http://dx.doi.org/10.1006/abbi.2001.2349.

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37

Marcinkeviciene, Jovita, Wenjun Jiang, Lisa M. Kopcho, Gregory Locke, Ying Luo, and Robert A. Copeland. "Enoyl-ACP Reductase (FabI) of Haemophilus influenzae: Steady-State Kinetic Mechanism and Inhibition by Triclosan and Hexachlorophene." Archives of Biochemistry and Biophysics 396, no. 2 (December 2001): 249. http://dx.doi.org/10.1006/abbi.2001.2706.

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38

Dutta, Debajyoti, Sudipta Bhattacharyya, Amlan Roychowdhury, Rupam Biswas, and Amit Kumar Das. "Crystal structure of hexanoyl-CoA bound to β-ketoacyl reductase FabG4 of Mycobacterium tuberculosis." Biochemical Journal 450, no. 1 (January 24, 2013): 127–39. http://dx.doi.org/10.1042/bj20121107.

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FabGs, or β-oxoacyl reductases, are involved in fatty acid synthesis. The reaction entails NADPH/NADH-mediated conversion of β-oxoacyl-ACP (acyl-carrier protein) into β-hydroxyacyl-ACP. HMwFabGs (high-molecular-weight FabG) form a phylogenetically separate group of FabG enzymes. FabG4, an HMwFabG from Mycobacterium tuberculosis, contains two distinct domains, an N-terminal ‘flavodoxintype’ domain and a C-terminal oxoreductase domain. The catalytically active C-terminal domain utilizes NADH to reduce β-oxoacyl-CoA to β-hydroxyacyl-CoA. In the present study the crystal structures of the FabG4–NADH binary complex and the FabG4–NAD+–hexanoyl-CoA ternary complex have been determined to understand the substrate specificity and catalytic mechanism of FabG4. This is the first report to demonstrate how FabG4 interacts with its coenzyme NADH and hexanoyl-CoA that mimics an elongating fattyacyl chain covalently linked with CoA. Structural analysis shows that the binding of hexanoyl-CoA within the active site cavity of FabG significantly differs from that of the C16 fattyacyl substrate bound to mycobacterial FabI [InhA (enoyl-ACP reductase)]. The ternary complex reveals that both loop I and loop II interact with the phosphopantetheine moiety of CoA or ACP to align the covalently linked fattyacyl substrate near the active site. Structural data ACP inhibition studies indicate that FabG4 can accept both CoA- and ACP-based fattyacyl substrates. We have also shown that in the FabG4 dimer Arg146 and Arg445 of one monomer interact with the C-terminus of the second monomer to play pivotal role in substrate association and catalysis.

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Marrakchi, H., Y. M. Zhang, and C. O. Rock. "Mechanistic diversity and regulation of Type II fatty acid synthesis." Biochemical Society Transactions 30, no. 6 (November 1, 2002): 1050–55. http://dx.doi.org/10.1042/bst0301050.

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Fatty acid biosynthesis is catalysed in most bacteria by a group of highly conserved proteins known as the Type II fatty acid synthase (FAS) system. The Type II system organization is distinct from its mammalian counterpart and offers several unique sites for selective inhibition by antibacterial agents. There has been remarkable progress in the understanding of the genetics, biochemistry and regulation of Type II FASs. One important advance is the discovery of the interaction between the fatty acid degradation regulator, FadR, and the fatty acid biosynthesis regulator, FabR, in the transcriptional control of unsaturated fatty acid synthesis in Escherichia coli. The availability of genomic sequences and high-resolution protein crystal structures has expanded our understanding of Type II FASs beyond the E. coli model system to a number of pathogens. The molecular diversity among the pathway enzymes is illustrated by the discovery of a new type of enoyl-reductase in Streptococcus pneumoniae [enoyl-acyl carrier protein (ACP) reductase II, FabK], the presence of two enoyl-reductases in Bacillus subtilis (enoyl-ACP reductases I and III, FabI and FabL), and the use of a new mechanism for unsaturated fatty acid formation in S. pneumoniae (trans-2-cis-3-enoyl-ACP isomerase, FabM). The solution structure of ACP from Mycobacterium tuberculosis revealed features common to all ACPs, but its extended C-terminal domain may reflect a specific interaction with very-long-chain intermediates.

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Thill, M., G. Pisa, and G. Isbary. "Therapieziele der neoadjuvanten Therapie – Präferenzen von Patientinnen mit frühem Mammakarzinom." Senologie - Zeitschrift für Mammadiagnostik und -therapie 14, no. 02 (June 2017): 99–105. http://dx.doi.org/10.1055/s-0043-105669.

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Zusammenfassung Hintergrund Therapeuten und Behörden betrachten eine pathologische Komplettremission (pCR) als eigenständigen und relevanten Endpunkt zur Beurteilung des klinischen Nutzens einer neoadjuvanten Therapie beim frühen Mammakarzinom. Die vorliegende Studie sollte untersuchen, welche Behandlungsziele einer neoadjuvanten Therapie Patientinnen selbst als relevant erachten. Material und Methodik Mithilfe der Analytical-Hierarchy-Process-(AHP-)Methode wurden Patientenpräferenzen zu Behandlungszielen einer neoadjuvanten Therapie quantitativ gewichtet. Alle Probandinnen hatten eine neoadjuvante Therapie in Form einer Chemotherapie und bei HER2-Positivität einer zielgerichteten Antikörpertherapie gegen HER2 aufgrund der Primärdiagnose eines Mammakarzinoms 12 – 36 Monaten vor der Befragung erhalten. Die Kriterien des Hierarchiemodells wurden in einer vorangehenden qualitativen Befragung identifiziert. Die Patientinneninterviews wurden von 4 erfahrenen Interviewerinnen durchgeführt. Ergebnisse An der quantitativen Befragung nahmen 41 Patientinnen teil, davon 15 (36,6 %) mit HER2-positiver Erkrankung. Das Erreichen einer pCR stellte für die Patientinnen das wichtigste Therapieziel vor krankheitsfreiem Überleben, Gesamtüberleben und der Möglichkeit einer brusterhaltenden Operation dar. Der Vermeidung von Nebenwirkungen wurde die geringste Bedeutung zugemessen. Beim Vergleich der Nebenwirkungen hatte für die Patientinnen Fatigue den höchsten Stellenwert vor Übelkeit und Haarausfall. Fazit Das Erreichen einer pathologischen Komplettremission stellt für Patientinnen ein eigenständiges relevantes und vorrangiges Ziel einer neoadjuvanten Therapie dar.

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Schmidt, Elizabeth Moreira dos Santos, and Peter David Eckersall. "Acute Phase Proteins as Markers of Infectious Diseases in small Animals / Proteini Akutne Faze Kao Markeri Infektivnih Bolesti Malih Životinja." Acta Veterinaria 65, no. 2 (June 1, 2015): 149–61. http://dx.doi.org/10.1515/acve-2015-0013.

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Abstract During the acute phase response, there is an increased production and release of certain proteins known as acute phase proteins (APPs) which can be produced by hepatocytes and peripheral tissues such as C-reactive protein (CRP), serum amyloid A (SAA), haptoglobin (Hp), alpha-1 acid glycoprotein (AGP). These proteins have been investigated as markers of various infectious diseases in small animals and the purpose of this review is to update the current knowledge about APPs in infectious diseases in dogs and cats.

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Min, Jun, Xiaoli Zhang, Lei Wang, Xia Zou, Qingye Zhang, and Jin He. "Mutational analysis of the interaction between a potential inhibitor luteolin and enoyl-ACP reductase (FabI) from Salmonella enterica." Journal of Molecular Catalysis B: Enzymatic 68, no. 2 (February 2011): 174–80. http://dx.doi.org/10.1016/j.molcatb.2010.10.007.

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Daryaee, Fereidoon, Andrew Chang, Johannes Schiebel, Yang Lu, Zhuo Zhang, Kanishk Kapilashrami, Stephen G. Walker, et al. "Correlating drug–target kinetics and in vivo pharmacodynamics: long residence time inhibitors of the FabI enoyl-ACP reductase." Chemical Science 7, no. 9 (2016): 5945–54. http://dx.doi.org/10.1039/c6sc01000h.

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44

Kleerebezem, M., M. Heutink, H. de Cock, and J. Tommassen. "The qmeA (ts) mutation of Escherichia coli is localized in the fabI gene, which encodes enoyl-ACP reductase." Research in Microbiology 147, no. 8 (January 1996): 609–13. http://dx.doi.org/10.1016/0923-2508(96)84016-2.

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45

Mehboob, Shahila, Jinhua Song, Kirk E. Hevener, Pin-Chih Su, Teuta Boci, Libby Brubaker, Lena Truong, et al. "Structural and biological evaluation of a novel series of benzimidazole inhibitors of Francisella tularensis enoyl-ACP reductase (FabI)." Bioorganic & Medicinal Chemistry Letters 25, no. 6 (March 2015): 1292–96. http://dx.doi.org/10.1016/j.bmcl.2015.01.048.

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46

Cummings, Jason E., Luke C. Kingry, Drew A. Rholl, Herbert P. Schweizer, Peter J. Tonge, and Richard A. Slayden. "The Burkholderia pseudomallei Enoyl-Acyl Carrier Protein Reductase FabI1 Is Essential forIn VivoGrowth and Is the Target of a Novel Chemotherapeutic with Efficacy." Antimicrobial Agents and Chemotherapy 58, no. 2 (November 25, 2013): 931–35. http://dx.doi.org/10.1128/aac.00176-13.

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ABSTRACTThe bacterial fatty acid biosynthesis pathway is a validated target for the development of novel chemotherapeutics. However, sinceBurkholderia pseudomalleicarries genes that encode both FabI and FabV enoyl-acyl carrier protein (ACP) reductase homologues, the enoyl-ACP reductase that is essential forin vivogrowth needs to be defined so that the correct drug target can be chosen for development. Accordingly, ΔfabI1, ΔfabI2, and ΔfabVknockout strains were constructed and tested in a mouse model of infection. Mice infected with a ΔfabI1strain did not show signs of morbidity, mortality, or dissemination after 30 days of infection compared to the wild-type and ΔfabI2and ΔfabVmutant strains that had times to mortality of 60 to 84 h. Although signs of morbidity and mortality of ΔfabI2and ΔfabVstrains were not significantly different from those of the wild-type strain, a slight delay was observed. A FabI1-specific inhibitor was used to confirm that inhibition of FabI1 results in reduced bacterial burden and efficacy in an acuteB. pseudomalleimurine model of infection. This work establishes that FabI1 is required for growth ofBurkholderia pseudomalleiin vivoand is a potential molecular target for drug development.

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Sharma, Shilpi, Shailendra Kumar Sharma, Rahul Modak, Krishanpal Karmodiya, Namita Surolia, and Avadhesha Surolia. "Mass Spectrometry-Based Systems Approach for Identification of Inhibitors of Plasmodium falciparum Fatty Acid Synthase." Antimicrobial Agents and Chemotherapy 51, no. 7 (May 7, 2007): 2552–58. http://dx.doi.org/10.1128/aac.00124-07.

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ABSTRACT The emergence of strains of Plasmodium falciparum resistant to the commonly used antimalarials warrants the development of new antimalarial agents. The discovery of type II fatty acid synthase (FAS) in Plasmodium distinct from the FAS in its human host (type I FAS) opened up new avenues for the development of novel antimalarials. The process of fatty acid synthesis takes place by iterative elongation of butyryl-acyl carrier protein (butyryl-ACP) by two carbon units, with the successive action of four enzymes constituting the elongation module of FAS until the desired acyl length is obtained. The study of the fatty acid synthesis machinery of the parasite inside the red blood cell culture has always been a challenging task. Here, we report the in vitro reconstitution of the elongation module of the FAS of malaria parasite involving all four enzymes, FabB/F (β-ketoacyl-ACP synthase), FabG (β-ketoacyl-ACP reductase), FabZ (β-ketoacyl-ACP dehydratase), and FabI (enoyl-ACP reductase), and its analysis by matrix-assisted laser desorption-time of flight mass spectrometry (MALDI-TOF MS). That this in vitro systems approach completely mimics the in vivo machinery is confirmed by the distribution of acyl products. Using known inhibitors of the enzymes of the elongation module, cerulenin, triclosan, NAS-21/91, and (−)-catechin gallate, we demonstrate that accumulation of intermediates resulting from the inhibition of any of the enzymes can be unambiguously followed by MALDI-TOF MS. Thus, this work not only offers a powerful tool for easier and faster throughput screening of inhibitors but also allows for the study of the biochemical properties of the FAS pathway of the malaria parasite.

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Tóthová, Csilla, Oskar Nagy, Veronika Nagyová, and Gabriel Kováč. "Changes in the Concentrations of Acute Phase Proteins in Calves during the first Month of Life / Promene Koncentracije Proteina Akutne Faze Tokom Prvog Meseca Života Teladi." Acta Veterinaria 65, no. 2 (June 1, 2015): 260–70. http://dx.doi.org/10.1515/acve-2015-0022.

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Abstract The objective of this study was to describe the physiological changes in the concentrations of acute phase proteins (APPs) in calves during the first month of life, including pre-, postcolostral and milk feeding period. Seven clinically healthy calves were used in this study. Calves received colostrum and whole milk from their dams. The first blood sampling was performed before colostrum intake (day 0) and then at 1, 2, 7, 14 and 30 days of age. Blood serum was analyzed for the concentrations of haptoglobin (Hp), serum amyloid A (SAA), α1-acid glycoprotein (AGP), ceruloplasmin (Cp), and albumin (Alb). The results showed significant changes in the serum concentrations of Hp, SAA and Cp (P<0.001, P<0.01, P<0.01). Their lowest concentrations were found after birth, and a gradual increase was observed after colostrum intake until day 7 of life. Another trend was observed in the concentrations of albumin with a more marked decrease of values 1 day after colostrum intake and subsequent significant increase of values until the end of the first month of age (P<0.001). Sampling time had no significant effect on the concentrations of AGP. The values observed at birth and on day 1 of life were relatively stable. The concentrations of AGP increased slightly from day 2 until the end of the first month of age. These results suggest that the concentrations of APPs in the neonatal period are influenced by colostrum intake and age. This should be taken into consideration for the precise interpretation of these analytes in young animals.

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Ozawa, Tomohiro, Sho Takahata, and Hideo Kitagawa. "Search for the Dual Inhibitors of Bacterial Enoyl-acyl Carrier Protein (ACP) Reductases (FabI and FabK) as Antibacterial Agents." Journal of Synthetic Organic Chemistry, Japan 70, no. 3 (2012): 265–75. http://dx.doi.org/10.5059/yukigoseikyokaishi.70.265.

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Ramnauth, Jailall, Mathew D. Surman, Peter B. Sampson, Bryan Forrest, Jeff Wilson, Emily Freeman, David D. Manning, et al. "2,3,4,5-Tetrahydro-1H-pyrido[2,3-b and e][1,4]diazepines as inhibitors of the bacterial enoyl ACP reductase, FabI." Bioorganic & Medicinal Chemistry Letters 19, no. 18 (September 2009): 5359–62. http://dx.doi.org/10.1016/j.bmcl.2009.07.094.

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