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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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1

Lahiri, Sujoy, Hyejung Park, Elad L. Laviad, Xuequan Lu, Robert Bittman, and Anthony H. Futerman. "Ceramide Synthesis Is Modulated by the Sphingosine Analog FTY720 via a Mixture of Uncompetitive and Noncompetitive Inhibition in an Acyl-CoA Chain Length-de pend ent Manner." Journal of Biological Chemistry 284, no. 24 (April 8, 2009): 16090–98. http://dx.doi.org/10.1074/jbc.m807438200.

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FTY720, a sphingosine analog, is in clinical trials as an immunomodulator. The biological effects of FTY720 are believed to occur after its metabolism to FTY720 phosphate. However, very little is known about whether FTY720 can interact with and modulate the activity of other enzymes of sphingolipid metabolism. We examined the ability of FTY720 to modulate de novo ceramide synthesis. In mammals, ceramide is synthesized by a family of six ceramide synthases, each of which utilizes a restricted subset of acyl-CoAs. We show that FTY720 inhibits ceramide synthase activity in vitro by noncompetitive inhibition toward acyl-CoA and uncompetitive inhibition toward sphinganine; surprisingly, the efficacy of inhibition depends on the acyl-CoA chain length. In cultured cells, FTY720 has a more complex effect, with ceramide synthesis inhibited at high (500 nm to 5 μm) but not low (<200 nm) sphinganine concentrations, consistent with FTY720 acting as an uncompetitive inhibitor toward sphinganine. Finally, electrospray ionization-tandem mass spectrometry demonstrated, unexpectedly, elevated levels of ceramide, sphingomyelin, and hexosylceramides after incubation with FTY720. Our data suggest a novel mechanism by which FTY720 might mediate some of its biological effects, which may be of mechanistic significance for understanding its mode of action.
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2

Mells, Jamie E., Ping P. Fu, Shvetank Sharma, Darin Olson, Lihong Cheng, Jeffrey A. Handy, Neeraj K. Saxena, Dan Sorescu, and Frank A. Anania. "Glp-1 analog, liraglutide, ameliorates hepatic steatosis and cardiac hypertrophy in C57BL/6J mice fed a Western diet." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 2 (January 2012): G225—G235. http://dx.doi.org/10.1152/ajpgi.00274.2011.

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The aims of this study were designed to determine whether liraglutide, a long-acting glucagon-like peptide, could reverse the adverse effects of a diet high in fat that also contained trans-fat and high-fructose corn syrup (ALIOS diet). Specifically, we examined whether treatment with liraglutide could reduce hepatic insulin resistance and steatosis as well as improve cardiac function. Male C57BL/6J mice were pair fed or fed ad libitum either standard chow or the ALIOS diet. After 8 wk the mice were further subdivided and received daily injections of either liraglutide or saline for 4 wk. Hyperinsulinemic-euglycemic clamp studies were performed after 6 wk, revealing hepatic insulin resistance. Glucose tolerance and insulin resistance tests were performed at 8 and 12 wk prior to and following liraglutide treatment. Liver pathology, cardiac measurements, blood chemistry, and RNA and protein analyses were performed. Clamp studies revealed hepatic insulin resistance after 6 wk of ALIOS diet. Liraglutide reduced visceral adiposity and liver weight ( P < 0.001). As expected, liraglutide improved glucose and insulin tolerance. Liraglutide improved hypertension ( P < 0.05) and reduced cardiac hypertrophy. Surprisingly, liver from liraglutide-treated mice had significantly higher levels of fatty acid binding protein, acyl-CoA oxidase II, very long-chain acyl-CoA dehydrogenase, and microsomal triglyceride transfer protein. We conclude that liraglutide reduces the harmful effects of an ALIOS diet by improving insulin sensitivity and by reducing lipid accumulation in liver through multiple mechanisms including, transport, and increase β-oxidation.
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3

Satoh, A. "Structure of the Transition State Analog of Medium-Chain Acyl-CoA Dehydrogenase. Crystallographic and Molecular Orbital Studies on the Charge-Transfer Complex of Medium-Chain Acyl-CoA Dehydrogenase with 3-Thiaoctanoyl-CoA." Journal of Biochemistry 134, no. 2 (August 1, 2003): 297–304. http://dx.doi.org/10.1093/jb/mvg143.

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4

Wang, Yutong, and John F. Oram. "Unsaturated Fatty Acids Phosphorylate and Destabilize ABCA1 through a Phospholipase D2 Pathway." Journal of Biological Chemistry 280, no. 43 (August 23, 2005): 35896–903. http://dx.doi.org/10.1074/jbc.m506210200.

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Abnormal high density lipoprotein (HDL) metabolism among patients with diabetes and insulin resistance may contribute to their increased risk of atherosclerosis. ATP-binding cassette transporter ABCA1 mediates the transport of cholesterol and phospholipids from cells to HDL apolipoproteins and thus modulates HDL levels and atherogenesis. Unsaturated fatty acids, which are elevated in diabetes, impair the ABCA1 pathway in cultured cells by destabilizing ABCA1 protein. Here we examined the cellular pathway that mediates the ABCA1 destabilizing effects of fatty acids. The long-chain acyl-CoA synthetase inhibitor triacsin C completely reversed fatty acid-induced ABCA1 destabilization, indicating that fatty acids need to be activated to their CoA derivatives to enhance ABCA1 degradation. Unsaturated but not saturated fatty acids stimulated phospholipase D (PLD) activity, the PLD inhibitor 1-butanol prevented the unsaturated fatty acid-induced reduction in ABCA1 levels, and the PLD2 activator mastoparan markedly reduced ABCA1 protein levels, implicating a role for PLD2 in the ABCA1 destabilizing effects of fatty acids. Unsaturated fatty acids and mastoparan increased phosphorylation of ABCA1 serines. PLD2 small interfering RNA abolished the ability of unsaturated fatty acids to inhibit lipid transport activity, to reduce protein levels, and to increase serine phosphorylation of ABCA1. The diacylglycerol analog oleoylacetylglycerol also reduced ABCA1 protein levels and increased its serine phosphorylation, suggesting that PLD2-generated diacylglycerols promote the destabilizing phosphorylation of ABCA1. These data provide evidence that intracellular unsaturated acyl-CoA derivatives destabilize ABCA1 by activating a PLD2 signaling pathway.
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5

Shockey, J. M., R. Rajasekharan, and J. D. Kemp. "Photoaffinity Labeling of Developing Jojoba Seed Microsomal Membranes with a Photoreactive Analog of Acyl-Coenzyme A (Acyl-CoA) (Identification of a Putative Acyl-CoA:Fatty Alcohol Acyltransferase." Plant Physiology 107, no. 1 (January 1, 1995): 155–60. http://dx.doi.org/10.1104/pp.107.1.155.

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6

Nishina, Y. "Molecular Mechanism of the Drop in the pKa of a Substrate Analog Bound to Medium-Chain Acyl-CoA Dehydrogenase: Implications for Substrate Activation." Journal of Biochemistry 134, no. 6 (December 1, 2003): 835–42. http://dx.doi.org/10.1093/jb/mvg209.

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7

van Loon, Luc J. C., Michaela Thomason-Hughes, Dumitru Constantin-Teodosiu, René Koopman, Paul L. Greenhaff, D. Grahame Hardie, Hans A. Keizer, Wim H. M. Saris, and Anton J. M. Wagenmakers. "Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans." American Journal of Physiology-Endocrinology and Metabolism 289, no. 3 (September 2005): E482—E493. http://dx.doi.org/10.1152/ajpendo.00092.2005.

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This study investigates the consequences of inhibition of adipose tissue lipolysis on skeletal muscle substrate use. Ten subjects were studied at rest and during exercise and subsequent recovery under normal, fasting conditions (control trial, CON) and following administration of a nicotinic acid analog (low plasma free fatty acid trial, LFA). Continuous [U-13C]palmitate and [6,6-2H2]glucose infusions were applied to quantify plasma free fatty acid (FFA) and glucose oxidation rates and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected to measure 1) fiber type-specific IMTG content; 2) allosteric regulators of hormone-sensitive lipase (HSL), glycogen phosphorylase, and pyruvate dehydrogenase; and 3) the phosphorylation status of HSL at Ser563 and Ser565. Administration of a nicotinic acid analog (acipimox) substantially reduced plasma FFA rate of appearance and subsequent plasma FFA concentrations ( P < 0.0001). At rest, this substantially reduced plasma FFA oxidation rates, which was compensated by an increase in the estimated IMTG use ( P < 0.05). During exercise, the progressive increase in FFA rate of appearance, uptake, and oxidation was prevented in the LFA trial and matched by greater IMTG and glycogen use. Differential phosphorylation of HSL or relief of its allosteric inhibition by long-chain fatty acyl-CoA could not explain the increase in muscle TG use, but there was evidence to support the contention that regulation may reside at the level of the glucose-fatty acid cycle. This study confirms the hypothesis that plasma FFA availability regulates both intramuscular lipid and glycogen use in vivo in humans.
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8

Heller, R., F. Bussolino, D. Ghigo, G. Garbarino, G. Pescarmona, U. Till, and A. Bosia. "Human endothelial cells are target for platelet-activating factor. II. Platelet-activating factor induces platelet-activating factor synthesis in human umbilical vein endothelial cells." Journal of Immunology 149, no. 11 (December 1, 1992): 3682–88. http://dx.doi.org/10.4049/jimmunol.149.11.3682.

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Abstract Platelet-activating factor (PAF), a phospholipid mediator with broad and potent biologic activities, is synthesized by several inflammatory cells including endothelial cells (EC). PAF is also an effective stimulating agent for EC leading to increased cell permeability and adhesivity. We examined the synthesis of PAF in human umbilical cord vein EC after stimulation of EC with PAF or with its nonmetabolizable analog 1-O-alkyl-2-N-methyl-carbamyl-sn-glycero-3-phosphocholine (C-PAF). PAF (1 to 100 nM) induced a dose- and time-dependent increase of PAF synthesis as detected by [3H]acetate incorporation into PAF fraction. Stimulation of PAF synthesis occurred via activation of the "remodeling pathway" as the 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine (lyso-PAF):acetyl-CoA acetyltransferase was dose-dependently increased after PAF treatment. The de novo pathway of PAF synthesis was not activated under these conditions. C-PAF was able to mimic the effect of authentic PAF on [3H] acetate incorporation. The inactive metabolite lyso-PAF (100 nM) had no influence on PAF synthesis in EC. CV-3988, BN 52021, and WEB 2086, potent and specific antagonists of PAF suppressed PAF effects on the remodeling pathway completely. The PAF- and C-PAF-induced [3H]PAF remained 93% cell-associated and was not degraded up to 10 min after stimulation. Characterization of the [3H]acetate-labeled material co-migrating with authentic PAF revealed that a significant proportion (approximately 57%) was actually 1-acyl-2-acetyl-sn-glycero-3-phosphocholine. PAF-induced PAF synthesis might be an important mechanism for amplifying original PAF signals and potentiating adhesive interactions of circulating cells with the endothelium.
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9

THORPE, Colin, Thomas L. CIARDELLI, Charles J. STEWART, and Theodor WIELAND. "Interaction of Long-Chain Acyl-CoA Analogs with Pig Kidney General Acyl-CoA Dehydrogenase." European Journal of Biochemistry 118, no. 2 (March 3, 2005): 279–82. http://dx.doi.org/10.1111/j.1432-1033.1981.tb06397.x.

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10

Costa, Catarina G., Lambertus Dorland, Ulbe Holwerda, Isabel Tavares de Almeida, Bwee-Tien Poll-The, Cornelis Jakobs та Marinus Duran. "Simultaneous analysis of plasma free fatty acids and their 3-hydroxy analogs in fatty acid β-oxidation disorders". Clinical Chemistry 44, № 3 (1 березня 1998): 463–71. http://dx.doi.org/10.1093/clinchem/44.3.463.

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Abstract We present a new derivatization procedure for the simultaneous gas chromatographic–mass spectrometric analysis of free fatty acids and 3-hydroxyfatty acids in plasma. Derivatization of target compounds involved trifluoroacetylation of hydroxyl groups and tert-butyldimethylsilylation of the carboxyl groups. This new derivatization procedure had the advantage of allowing the complete baseline separation of free fatty acids and 3-hydroxyfatty acids while the superior gas chromatographic and mass spectrometric properties of tert-butyldimethylsilyl derivatives remained unchanged, permitting a sensitive analysis of the target compounds. Thirty-nine plasma samples from control subjects and patients with known defects of mitochondrial fatty acid β-oxidation were analyzed. A characteristic increase of long-chain 3-hydroxyfatty acids was observed for all of the long-chain 3-hydroxyacyl-CoA dehydrogenase-deficient and mitochondrial trifunctional protein-deficient plasma samples. For medium-chain acyl-CoA dehydrogenase deficiency and very-long-chain acyl-CoA dehydrogenase deficiency, decenoic and tetradecenoic acids, respectively, were the main abnormal fatty acids, whereas the multiple acyl-CoA dehydrogenase-deficient patients showed variable increases of these unusual intermediates. The results showed that this selective and sensitive method is a powerful tool in the diagnosis and monitoring of mitochondrial fatty acid β-oxidation disorders.
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11

Haeffnergormley, L., J. G. Cummings, and C. Thorpe. "S-2-Bromo-Acyl-CoA Analogs Are Affinity Labels for the Medium-Chain Acyl-CoA Dehydrogenase from Pig-Kidney." Archives of Biochemistry and Biophysics 317, no. 2 (March 1995): 479–86. http://dx.doi.org/10.1006/abbi.1995.1191.

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12

RAJASEKHARAN, Ram, Vasanthi NACHIAPPAN, and Hiranya S. ROYCHOWDHURY. "Photolabeling of soybean microsomal membrane proteins with photoreactive acyl-CoA analogs." European Journal of Biochemistry 220, no. 3 (March 1994): 1013–18. http://dx.doi.org/10.1111/j.1432-1033.1994.tb18706.x.

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13

Powell, Patricia J., Sze Mei Lau, David Killian, and Colin Thorpe. "Interaction of acyl coenzyme A substrates and analogs with pig kidney medium-chain acyl-CoA dehydrogenase." Biochemistry 26, no. 12 (June 16, 1987): 3704–10. http://dx.doi.org/10.1021/bi00386a066.

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14

Grayson, Neile A., and Richard B. Westkaemper. "Stable analogs of acyl adenylates. Inhibition of acetyl- and acyl-coa synthetase by adenosine 5′-alkylphosphates." Life Sciences 43, no. 5 (January 1988): 437–44. http://dx.doi.org/10.1016/0024-3205(88)90523-1.

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15

Coleman, James P., L. Lynn Hudson, Susan L. McKnight, John M. Farrow, M. Worth Calfee, Claire A. Lindsey, and Everett C. Pesci. "Pseudomonas aeruginosa PqsA Is an Anthranilate-Coenzyme A Ligase." Journal of Bacteriology 190, no. 4 (December 14, 2007): 1247–55. http://dx.doi.org/10.1128/jb.01140-07.

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ABSTRACT Pseudomonas aeruginosa is an opportunistic human pathogen which relies on several intercellular signaling systems for optimum population density-dependent regulation of virulence genes. The Pseudomonas quinolone signal (PQS) is a 3-hydroxy-4-quinolone with a 2-alkyl substitution which is synthesized by the condensation of anthranilic acid with a 3-keto-fatty acid. The pqsABCDE operon has been identified as being necessary for PQS production, and the pqsA gene encodes a predicted protein with homology to acyl coenzyme A (acyl-CoA) ligases. In order to elucidate the first step of the 4-quinolone synthesis pathway in P. aeruginosa, we have characterized the function of the pqsA gene product. Extracts prepared from Escherichia coli expressing PqsA were shown to catalyze the formation of anthraniloyl-CoA from anthranilate, ATP, and CoA. The PqsA protein was purified as a recombinant His-tagged polypeptide, and this protein was shown to have anthranilate-CoA ligase activity. The enzyme was active on a variety of aromatic substrates, including benzoate and chloro and fluoro derivatives of anthranilate. Inhibition of PQS formation in vivo was observed for the chloro- and fluoroanthranilate derivatives, as well as for several analogs which were not PqsA enzymatic substrates. These results indicate that the PqsA protein is responsible for priming anthranilate for entry into the PQS biosynthetic pathway and that this enzyme may serve as a useful in vitro indicator for potential agents to disrupt quinolone signaling in P. aeruginosa.
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16

Johnson, Jeffrey K., Zhi Xin Wang, and D. K. Srivastava. "Mechanistic investigation of medium-chain fatty acyl-CoA dehydrogenase utilizing (3-indolpropionyl/acryloyl-CoA as chromophoric substrate analogs." Biochemistry 31, no. 43 (November 1992): 10564–75. http://dx.doi.org/10.1021/bi00158a020.

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17

Kwon, Byoung-Mog, Sook-Hee Ro, Mi-Kyoung Kim, Ji-Youn Nam, Hyun-Ju Jung, Ihn-Rhan Lee, Young-Kook Kim, and Song-Hae Bok. "Polyacetylene Analogs, Isolated from Hairy Roots ofPanax ginseng, Inhibit Acyl-CoA : Cholesterol Acyltransferase." Planta Medica 63, no. 06 (December 1997): 552–53. http://dx.doi.org/10.1055/s-2006-957763.

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18

Pace, C. P., and M. T. Stankovich. "Oxidation-Reduction Properties of Short-Chain Acyl-CoA Dehydrogenase: Effects of Substrate Analogs." Archives of Biochemistry and Biophysics 313, no. 2 (September 1994): 261–66. http://dx.doi.org/10.1006/abbi.1994.1386.

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19

Johnson, Bruce D., and Marian T. Stankovich. "Influence of two substrate analogs on thermodynamic properties of medium-chain acyl-CoA dehydrogenase." Biochemistry 32, no. 40 (October 12, 1993): 10779–85. http://dx.doi.org/10.1021/bi00091a032.

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20

Srividya, Narayanan, Iris Lange, Michael Hartmann, Qunrui Li, Maryam Mirzaei, and Bernd Markus Lange. "Biochemical characterization of acyl activating enzymes for side chain moieties of Taxol and its analogs." Journal of Biological Chemistry 295, no. 15 (February 20, 2020): 4963–73. http://dx.doi.org/10.1074/jbc.ra120.012663.

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Taxol (paclitaxel) is a very widely used anticancer drug, but its commercial sources mainly consist of stripped bark or suspension cultures of members of the plant genus Taxus. Taxol accumulates as part of a complex mixture of chemical analogs, termed taxoids, which complicates its production in pure form, highlighting the need for metabolic engineering approaches for high-level Taxol production in cell cultures or microbial hosts. Here, we report on the characterization of acyl-activating enzymes (AAEs) that catalyze the formation of CoA esters of different organic acids relevant for the N-substitution of the 3-phenylisoserine side chain of taxoids. On the basis of similarities to AAE genes of known function from other organisms, we identified candidate genes in publicly available transcriptome data sets obtained with Taxus × media. We cloned 17 AAE genes, expressed them heterologously in Escherichia coli, purified the corresponding recombinant enzymes, and performed in vitro assays with 27 organic acids as potential substrates. We identified TmAAE1 and TmAAE5 as the most efficient enzymes for the activation of butyric acid (Taxol D side chain), TmAAE13 as the best candidate for generating a CoA ester of tiglic acid (Taxol B side chain), TmAAE3 and TmAAE13 as suitable for the activation of 4-methylbutyric acid (N-debenzoyl-N-(2-methylbutyryl)taxol side chain), TmAAE15 as a highly efficient candidate for hexanoic acid activation (Taxol C side chain), and TmAAE4 as suitable candidate for esterification of benzoic acid with CoA (Taxol side chain). This study lays important groundwork for metabolic engineering efforts aimed at improving Taxol production in cell cultures.
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21

Johnson, Bruce D., Gina J. Mancini-Samuelson, and Marian T. Stankovich. "Effect of transition-state analogs on the redox properties of medium-chain acyl-CoA dehydrogenase." Biochemistry 34, no. 21 (May 30, 1995): 7047–55. http://dx.doi.org/10.1021/bi00021a016.

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22

Brockhausen, Inka, Dileep G. Nair, Min Chen, Xiaojing Yang, John S. Allingham, Walter A. Szarek, and Tassos Anastassiades. "Human acetyl-CoA:glucosamine-6-phosphate N-acetyltransferase 1 has a relaxed donor specificity and transfers acyl groups up to four carbons in length." Biochemistry and Cell Biology 94, no. 2 (April 2016): 197–204. http://dx.doi.org/10.1139/bcb-2015-0115.

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Glucosamine-6-phosphate N-acetyltransferase1 (GNA1) catalyses the transfer of an acetyl group from acetyl coenzyme A (AcCoA) to glucosamine-6-phosphate (GlcN6P) to form N-acetylglucosamine-6-phosphate (GlcNAc6P), which is an essential intermediate in UDP-GlcNAc biosynthesis. An analog of GlcNAc, N-butyrylglucosamine (GlcNBu) has shown healing properties for bone and articular cartilage in animal models of arthritis. The goal of this work was to examine whether GNA1 has the ability to transfer a butyryl group from butyryl-CoA to GlcN6P to form GlcNBu6P, which can then be converted to GlcNBu. We developed fluorescent and radioactive assays and examined the donor specificity of human GNA1. Acetyl, propionyl, n-butyryl, and isobutyryl groups were all transferred to GlcN6P, but isovaleryl-CoA and decanoyl-CoA did not serve as donor substrates. Site-specific mutants were produced to examine the role of amino acids potentially affecting the size and properties of the AcCoA binding pocket. All of the wild type and mutant enzymes showed activities of both acetyl and butyryl transfer and can therefore be used for the enzymatic synthesis of GlcNBu for biomedical applications.
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23

Rodríguez, Sergio, Francisco Camps, and Gemma Fabriàs. "Inhibition of the acyl-CoA desaturases involved in the biosynthesis of Spodoptera littoralis sex pheromone by analogs of 10,11-methylene-10-tetradecenoic acid." Insect Biochemistry and Molecular Biology 34, no. 3 (March 2004): 283–89. http://dx.doi.org/10.1016/j.ibmb.2003.11.003.

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24

Lee, T. C., Y. Uemura, and F. Snyder. "A novel CoA-independent transacetylase produces the ethanolamine plasmalogen and acyl analogs of platelet-activating factor (PAF) with PAF as the acetate donor in HL-60 cells." Journal of Biological Chemistry 267, no. 28 (October 1992): 19992–20001. http://dx.doi.org/10.1016/s0021-9258(19)88655-6.

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25

Takahashi, Shunya, Keiko Hasumi, Atsushi Ohnishi, Hiroyuki Koshino, and Shogo Matsumoto. "Synthesis and biological activities of analogs of d-glucosyl-l-tyrosine, a humoral factor that stimulates transcription of the acyl-CoA binding protein in the pheromone gland of the Silkmoth, Bombyx mori." Bioorganic & Medicinal Chemistry 15, no. 1 (January 1, 2007): 97–103. http://dx.doi.org/10.1016/j.bmc.2006.10.008.

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26

Manesis, Anastasia C., Alina Yerbulekova, Jason Shearer, and Hannah S. Shafaat. "Thioester synthesis by a designed nickel enzyme models prebiotic energy conversion." Proceedings of the National Academy of Sciences 119, no. 30 (July 18, 2022). http://dx.doi.org/10.1073/pnas.2123022119.

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The formation of carbon–carbon bonds from prebiotic precursors such as carbon dioxide represents the foundation of all primordial life processes. In extant organisms, this reaction is carried out by the carbon monoxide dehydrogenase (CODH)/acetyl coenzyme A synthase (ACS) enzyme, which performs the cornerstone reaction in the ancient Wood–Ljungdahl metabolic pathway to synthesize the key biological metabolite, acetyl-CoA. Despite its significance, a fundamental understanding of this transformation is lacking, hampering efforts to harness analogous chemistry. To address these knowledge gaps, we have designed an artificial metalloenzyme within the azurin protein scaffold as a structural, functional, and mechanistic model of ACS. We demonstrate the intermediacy of the Ni I species and requirement for ordered substrate binding in the bioorganometallic carbon–carbon bond-forming reaction from the one-carbon ACS substrates. The electronic and geometric structures of the nickel-acetyl intermediate have been characterized using time-resolved optical, electron paramagnetic resonance, and X-ray absorption spectroscopy in conjunction with quantum chemical calculations. Moreover, we demonstrate that the nickel-acetyl species is chemically competent for selective acyl transfer upon thiol addition to biosynthesize an activated thioester. Drawing an analogy to the native enzyme, a mechanism for thioester generation by this ACS model has been proposed. The fundamental insight into the enzymatic process provided by this rudimentary ACS model has implications for the evolution of primitive ACS-like proteins. Ultimately, these findings offer strategies for development of highly active catalysts for sustainable generation of liquid fuels from one-carbon substrates, with potential for broad applications across diverse fields ranging from energy storage to environmental remediation.
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