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D2078G
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naturally occuring mutation that confers resistance to ACCase inhibitors fenoxaprop, clodinafop, haloxyfop, cycloxydim, clethodim
G2096A
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naturally occuring mutation that confers resistance to ACCase inhibitors fenoxaprop, clodinafop and haloxyfop, and probably also to clethodim
I1781L
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naturally occuring mutation that confers resistance to ACCase inhibitors fenoxaprop, clodinafop and haloxyfop, and to cycloxydim, and probably also to clethodim
I1781L/W2027C/I2041N/D2078G/G2096A
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naturally occuring mutant ACCase isoforms in Alopecurus myosuroides show resistance to five ACCase inhibitors, i.e. fenoxaprop, clodinafop, haloxyfop, cycloxydim, clethodim, phenotypes, overview
I2041N
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naturally occuring mutation that confers resistance to ACCase inhibitors fenoxaprop, clodinafop and haloxyfop
W2027C
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naturally occuring mutation that confers resistance to ACCase inhibitors fenoxaprop, clodinafop and haloxyfop
G199S
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construction and isolation of a mutant strain less sensitive to moiramide B derivative cpd2 compared to the wild-type strain
C5493T
the single nucleotide polymorphism is associated with fat yield but not with a structural change in the enzyme
S1263A
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site-directed mutagenesis
C2088A
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mutation endowing clethodim resistance
D2078G
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mutation endowing clethodim resistance
Q1756E
Q3HWZ7, Q3HWZ8, Q3HWZ9, Q3HX00, Q3HX01, Q3HX02, Q3HX04, Q3HX05, Q3HX07, Q3HX09, Q3HX10 resistant to sethoxydim
K73E
mutation in the biotin carboxylase domain dimer interface, loss of catalytic activity
K73R
the mutant shows resistance to soraphen A
L1705I
site-directed mutagenesis, the mutant enzyme shows 100fold decreased activity and 10fold increased Km for malonyl-CoA, but unaltered Ki for haloxyfop compared to the wild-type enzyme
P1760S/I1762L/M1765V/E1919Q/P1920A/H1925F/Q2028E/M2030T/G2032E
humanized mutant of yeast CT domain is generated by replacing nine active site residues of yeast CT domain with corresponding human ACC2 CT domain residues. This humanized yeast CT domain (yCT-H9) exhibits an inhibitor sensitivity profile similar to that of human ACC while maintaining high recombinant expression yields and robust crystallizability
Q608
mutation has little effect on catalysis
R656E
mutation has little effect on catalysis
R76E
mutation in the biotin carboxylase domain dimer interface, loss of catalytic activity
S1157A
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mutation in potential site of phosphorylation, results in 9fold higher specific activity following glucose depletion
V1967I
site-directed mutagenesis, the mutant enzyme shows 100fold decreased activity and 10fold increased Km for malonyl-CoA, but unaltered Ki for haloxyfop compared to the wild-type enzyme
W487A
mutation in the biotin carboxylase domain dimer interface, loss of catalytic activity
G196S
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construction and isolation of a mutant strain less sensitive to moiramide B derivative (E)-3-benzo[1,3]dioxol-5-yl-N-[(S)-2-[(S)-2-methyl-1-((3R,4S)-4-methyl-2,5-dioxo-pyrrolidine-3-carbonyl)-propylcarbamoyl]-1-phenyl-ethyl]-acrylamide compared to the wild-type strain
I420D
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site-directed mutagenesis of AccB, exchange of a single amino acid results in interconversion of substrate specificity of acetyl-CoA carboxylase ACC and propionyl-CoA carboxylase, PCC, EC 6.4.1.3, thus the mutant enzyme does not utilize acetyl-CoA as a substrate, but propionyl-CoA
I1781L
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mutation endowing clethodim resistance
I1781L
Q3HWZ7, Q3HWZ8, Q3HWZ9, Q3HX00, Q3HX01, Q3HX02, Q3HX04, Q3HX05, Q3HX07, Q3HX09, Q3HX10 resistant to sethoxydim
L1705I/V1967I
site-directed mutagenesis, the mutant enzyme shows 100fold decreased activity and 10fold increased Km for malonyl-CoA, but unaltered Ki for haloxyfop compared to the wild-type enzyme
L1705I/V1967I
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the mutant is not more sensitive to FOP herbicides than the wild-type enzyme
additional information
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five mutant ACCase isoforms in black-grass: Leu1781, Cys2027, Asn2041, Gly2078, and Ala2096, genotyping, overview
additional information
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construction of transgenic potato plants by overexpression of the Arabidopsis thaliana isozyme ACC1 in the amyloplast of Solanum tuberosum tubers leads to an increased fatty acid synthesis and a 5fold increased amount of triacylglycerol in the tubers
additional information
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missense mutation of the biotin carboxylase domain located at the active site disrupts catalysis
additional information
mutations gurke, gk-SC allele, and pasticcino3, pas3-1 and pas3-2 alleles, affect cell division and the bilateral symmetry due to severe defects in the apical region, the mutations are allelic to the lethal acc1 mutation, acc1-1 and acc1-2 alleles, leading to a similar phenotype in embryos, altered fatty acid composition, the phenotype can be partially complemented by malonate, overview
additional information
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a constructed truncation mutant of subunit AccB comprising the 68 N-terminal residues is sufficient for negative regulation of accBC operon transcription, an accA and accB null mutant strain expressing the accB gene of Rhizobium trifolii is not reduced in growth under conditions that result in highly reduced growth for the wild-type strain
additional information
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construction and isolation of mutant a strain resistant to moiramide B derivative (E)-3-benzo[1,3]dioxol-5-yl-N-[(S)-2-[(S)-2-methyl-1-((3R,4S)-4-methyl-2,5-dioxo-pyrrolidine-3-carbonyl)-propylcarbamoyl]-1-phenyl-ethyl]-acrylamide
additional information
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construction and isolation of mutant a strain resistant to moiramide B derivative (E)-3-benzo[1,3]dioxol-5-yl-N-[(S)-2-[(S)-2-methyl-1-((3R,4S)-4-methyl-2,5-dioxo-pyrrolidine-3-carbonyl)-propylcarbamoyl]-1-phenyl-ethyl]-acrylamide
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additional information
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deletion of downstream sequences affects the response to 3,5,3'-triiodothyronine
additional information
deletion of the N-terminal 148 hydrophobic amino acids to enhance the solubility of heterologous protein expressed in Bomby mori. Expression of the deletion mutant leads to a high yield of recombinant protein
additional information
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deletion of the N-terminal 148 hydrophobic amino acids to enhance the solubility of heterologous protein expressed in Bomby mori. Expression of the deletion mutant leads to a high yield of recombinant protein
additional information
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ACC2 knockout mutant mice are protected against diet-induced obesity and diabetes and show a 80% increased palmitate oxidation level in adipocytes which remains increased in presence of insulin, also the glucose oxidation is 2fold increased in mutant mice compared to wild-type mice
additional information
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ACC2-deficient mice show continous fatty acid oxidation and reduced body weight and body fat
additional information
downregulation of the enzyme by siRNA transfected into the INS-1-derived cell line 832/13 affects insulin secretion, the enzyme activity in 832/13 cells and islets is reduced by 46-80% compared to the untreated cells, and glucose-stimulated insulin secretion is reduced by 70% in 832/13 cells and by 33% in islets, phenotypes, overview
additional information
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enzyme deletion is lethal
additional information
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mutants of genes HFA1 and ACC1 shows different phenotypes and the enzymes cannot complement each other, the mitochondrial enzyme Hfa1p disruption mutant strain shows about 90% reduced lipoic acid concentration and does not grow on lactate or glycerol, complementation of hfa1 null mutants require full length HFA1 DNA including the mitochondrial targeting sequence, without the sequence the cDNA encoding the mitochondrial enzyme can complement the cytoplasmic acc1-defective mutant, overview
additional information
deletion of the alpha-helical hairpin (alpha8-alpha9, residues 940-972) in domain AC1 or the beta4A-beta4B loop in the C domain of carboxyltransferase (residues 1902-1916) abolishes the catalytic activity
additional information
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deletion of the alpha-helical hairpin (alpha8-alpha9, residues 940-972) in domain AC1 or the beta4A-beta4B loop in the C domain of carboxyltransferase (residues 1902-1916) abolishes the catalytic activity
additional information
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mutants of genes HFA1 and ACC1 shows different phenotypes and the enzymes cannot complement each other, the mitochondrial enzyme Hfa1p disruption mutant strain shows about 90% reduced lipoic acid concentration and does not grow on lactate or glycerol, complementation of hfa1 null mutants require full length HFA1 DNA including the mitochondrial targeting sequence, without the sequence the cDNA encoding the mitochondrial enzyme can complement the cytoplasmic acc1-defective mutant, overview
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additional information
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construction of transgenic potato plants by overexpression of the Arabidopsis thaliana isozyme ACC1 in the amyloplast of tubers leads to an increased fatty acid synthesis and a 5fold increased amount of triacylglycerol in the tubers, up to 10fold increased enzyme activity in transgenic plants
additional information
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formation of chimeric complexes with subunits, wild-type and mutant D422I, of the propionyl-CoA carboxylase, PCC, EC 6.4.1.3, and with mutant subunit AccB I420D of the acetyl-CoA carboxylase