1.3.3.6: acyl-CoA oxidase
This is an abbreviated version!
For detailed information about acyl-CoA oxidase, go to the full flat file.
Word Map on EC 1.3.3.6
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1.3.3.6
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beta-oxidation
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proliferator-activated
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ppars
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carnitine
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catalase
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triglyceride
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hepatocytes
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cholesterol
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pparalpha
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thiolase
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palmitoyltransferase
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steatosis
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adipose
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proliferators
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high-fat
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sterol
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clofibrate
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hypolipidemic
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enoyl-coa
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3-ketoacyl-coa
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adrenoleukodystrophy
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ciprofibrate
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zellweger
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fenofibrate
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refsum
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bezafibrate
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very-long-chain
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perfluorooctanoic
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cyp4a1
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plasmalogens
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pristanic
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srebp-1c
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3-hydroxyacyl-coa
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phytanic
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fibrates
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cyanide-insensitive
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rxralpha
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vlcfas
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nafenopin
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lignoceric
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medicine
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pmp70
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rhizomelic
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3-oxoacyl-coa
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nutrition
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degradation
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analysis
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2,4-dienoyl-coa
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omega-oxidation
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biotechnology
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di2-ethylhexylphthalate
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clofibrate-treated
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peroxisome-proliferator
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l-fabp
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peroxins
- 1.3.3.6
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beta-oxidation
-
proliferator-activated
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ppars
- carnitine
- catalase
- triglyceride
- hepatocytes
- cholesterol
- pparalpha
-
thiolase
- palmitoyltransferase
- steatosis
- adipose
- proliferators
-
high-fat
- sterol
- clofibrate
-
hypolipidemic
- enoyl-coa
- 3-ketoacyl-coa
- adrenoleukodystrophy
- ciprofibrate
- zellweger
- fenofibrate
- refsum
- bezafibrate
-
very-long-chain
-
perfluorooctanoic
- cyp4a1
- plasmalogens
-
pristanic
- srebp-1c
- 3-hydroxyacyl-coa
-
phytanic
-
fibrates
-
cyanide-insensitive
-
rxralpha
-
vlcfas
-
nafenopin
-
lignoceric
- medicine
- pmp70
-
rhizomelic
- 3-oxoacyl-coa
- nutrition
- degradation
- analysis
-
2,4-dienoyl-coa
-
omega-oxidation
- biotechnology
-
di2-ethylhexylphthalate
-
clofibrate-treated
-
peroxisome-proliferator
-
l-fabp
- peroxins
Reaction
Synonyms
3alpha,7alpha, 12alpha-trihydroxy-5beta-cholestanoyl-CoA oxidase, ACO, ACO I, ACO-A1, ACO-I, ACO-II, ACOX, ACOX-1, ACOX-1.1, ACOX-1.2, ACOX-1.3, ACOX-2, ACOX-3, ACOX1, ACOX1-3I, ACOX1a, ACOX1b, ACOX1–3II, ACOX2, ACOX3, ACX, ACX1, ACX1.2, ACX2, ACX3, ACX4, ACX5, acyl coenzyme A oxidase, acyl-CoA dehydrogenase, Acyl-CoA oxidase, acyl-CoA oxidase 1, acyl-CoA oxidase 1a, acyl-CoA oxidase 1b, acyl-CoA oxidase 2, acyl-CoA oxidase 4, acyl-CoA oxidase I, acyl-CoA oxidase-1, acyl-CoA oxidase-II, acyl-CoA-oxidase, acyl-coenzyme A oxidase, acyl-coenzyme A oxidase 1, acyl-coenzyme A oxidase 4, acyl-coenzyme A: oxygen oxidoreductase, AOX, AOX1, AOX2, Aox2p, AOX3, Aox3p, AOX4, aoxA, Aoxp, AtACX1, AtACX2, AtACX3, AtSACX, BRCACox, CrACX2, Cre05.g232002, fatty acyl-CoA oxidase, fatty acyl-coenzyme A oxidase, long chain acyl-CoA oxidase, long chain fatty acyl coenzyme A oxidase, long chain fatty acyl-CoA oxidase, long-chain-specific acyl-CoA oxidase 1, MCAD Y375K, MCOX, oxidase, acyl-coenzyme A, palmitoyl-CoA oxidase, peroxisomal acyl-coenzyme A oxidase, Peroxisomal fatty acyl-CoA oxidase, POX1, Pox1p, POX4, PpACX1, Pristanoyl-CoA oxidase, SCOX, short chain-specific acyl-CoA oxidase, short-chain acyl-CoA oxidase, straight chain acyl-CoA oxidase, straight-chain acyl-coenzyme A oxidase, THCA-CoA oxidase, THCCox, Trihydroxycoprostanoyl-CoA oxidase
ECTree
1.3.3.6 acyl-CoA oxidaseAdvanced search results
results (
results (Engineering
Engineering on EC 1.3.3.6 - acyl-CoA oxidase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
G432R
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conversion of Aox from component A to components B and C is completely prevented at both 30°C and 37°C
G231V
the mutation in combination with skipping of exon 13 leads to peroxisomal acyl-CoA oxidase deficiency
R210H
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naturally occuring apparent homozygous missense mutation c.629G/A of SCOX in a peroxisomal acyl-coenzyme A oxidase deficiency patient
C159T
C159T/C420S
activity less than one tenth of that of the wild type
C159T/C424V
activity less than one tenth of that of the wild type
C420S
C420S/424V
activity less than one tenth of that of the wild type
C424V
C159T
C420S
C424V
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looses more than half of the activity after incubation with N-Ethylmaleimide
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E421A
E421D
E421Q
Y232F
the mutant shows reduced activity compared to the wild type enzyme
Y232G
the mutant shows reduced activity compared to the wild type enzyme
Y232S
the mutant shows reduced activity compared to the wild type enzyme
Y401F
the mutant shows reduced activity compared to the wild type enzyme
T138I
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compromised in wound-response signaling owing to a deficiency in jasmonic acid synthesis, FAD is not bound in the mutant protein
additional information
C159T
exhibits 60% activity of the wild-type enzyme, looses more than half of the activity after incubation with N-ethylmaleimide
C159T
60% activity compared to the wild type enzyme and shows increased sensitivity to N-ethylmaleimide
C420S
exhibits 41% activity of the wild-type enzyme, retains about 90% of the activity after incubation with N-ethylmaleimide
C420S
41% activity compared to the wild type enzyme and shows increased sensitivity to N-ethylmaleimide
C424V
looses more than half of the activity after incubation with N-Ethylmaleimide
C424V
98% activity compared to the wild type enzyme and shows increased sensitivity to N-ethylmaleimide
C159T
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exhibits 60% activity of the wild-type enzyme, looses more than half of the activity after incubation with N-ethylmaleimide
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C159T
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60% activity compared to the wild type enzyme and shows increased sensitivity to N-ethylmaleimide
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C420S
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exhibits 41% activity of the wild-type enzyme, retains about 90% of the activity after incubation with N-ethylmaleimide
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C420S
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41% activity compared to the wild type enzyme and shows increased sensitivity to N-ethylmaleimide
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E421D
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Km-value for octanoyl-CoA is 1.23fold higher than the wild-type value. The turnover number for octanoyl-CoA is 1.6fold lower than activity of the wild-type enzyme
E421D
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isomerase activity is decreased for all tested cis- and trans-substrates compared with that of wild-type enzyme
additional information
acx1-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is unaltered in the acx1-1 mutant, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx1-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype, wound-induced increase in jasmonic acid is only compromised in the acx1-1 mutant
additional information
acx1-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is unaltered in the acx1-1 mutant, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx1-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype, wound-induced increase in jasmonic acid is only compromised in the acx1-1 mutant
additional information
acx1-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is unaltered in the acx1-1 mutant, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx1-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype, wound-induced increase in jasmonic acid is only compromised in the acx1-1 mutant
additional information
acx1-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is unaltered in the acx1-1 mutant, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx1-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype, wound-induced increase in jasmonic acid is only compromised in the acx1-1 mutant
additional information
acx2-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is slightly delayed in the acx2-1 mutant, with 3-day-old acx2-1 seedlings accumulating long-chain acyl-CoAs, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx2-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype
additional information
acx2-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is slightly delayed in the acx2-1 mutant, with 3-day-old acx2-1 seedlings accumulating long-chain acyl-CoAs, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx2-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype
additional information
acx2-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is slightly delayed in the acx2-1 mutant, with 3-day-old acx2-1 seedlings accumulating long-chain acyl-CoAs, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx2-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype
additional information
acx2-1 mutant, acx1-1 acx2-1 double mutant, lipid catabolism during germination and early post-germinative growth is slightly delayed in the acx2-1 mutant, with 3-day-old acx2-1 seedlings accumulating long-chain acyl-CoAs, seedlings of the double mutant acx1-1 acx2-1 are unable to catabolize seed storage lipid, accumulate long-chain acyl-CoAs, and are unable to establish photosynthetic competency in the absence of an exogenous carbon supply, germination frequency of the double mutant acx1-1 acx2-1 is significantly reduced compared with wild-type seeds, is improved by dormancy-breaking treatments, the acx2-1 and acx1-2 acx2-1 double mutants exhibit a sucrose-independent germination phenotype
additional information
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mutants defective in ACX1, ACX3, or ACX4 have reduced fatty acyl-CoA oxidase activity, acx1 acx2 double mutants display enhanced indole-3-butyric acid resistance and are sucrose dependent during seedling development, acx1 acx3 and acx1 acx5 double mutants display enhanced indole-3-butyric acid resistance but remain sucrose independent
additional information
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the ibr3-1 acx3-4 double mutant shows greatly enhanced indole-3-butyric acid resistance
additional information
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generation of higher-order acx mutants, the acx3acx4Col and acx1acx3acx4Col mutants are viable, enzyme activity in these mutants is significantly reduced on a range of substrates compared to the wild-type
additional information
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generation of higher-order acx mutants, the acx3acx4Col and acx1acx3acx4Col mutants are viable, enzyme activity in these mutants is significantly reduced on a range of substrates compared to the wild-type
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additional information
screening of a Chlamydomonas reinhardtii insertional mutant library identifies a strain strongly impaired in oil remobilization and defective in Cre05.g232002 (CrACX2), Nb7D4 is disrupted in gene Cre05.g232002. The mutant strain is defective in beta-oxidation of fatty acids and cannot grow on oleic acid. Turnover of fatty acids during diurnal growth is compromised in cracx2 mutant cells. Cellular oil content is increased by 20% in cracx2 mutants during N starvation. Phenotype, overview
additional information
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screening of a Chlamydomonas reinhardtii insertional mutant library identifies a strain strongly impaired in oil remobilization and defective in Cre05.g232002 (CrACX2), Nb7D4 is disrupted in gene Cre05.g232002. The mutant strain is defective in beta-oxidation of fatty acids and cannot grow on oleic acid. Turnover of fatty acids during diurnal growth is compromised in cracx2 mutant cells. Cellular oil content is increased by 20% in cracx2 mutants during N starvation. Phenotype, overview
additional information
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ACOX1-/- mice show twofold increased expression of isozyme ACOX1a compared to wild-type mice, ACOX1b-/- and ACOX1a-/- phenotypes, overview. Expression of human ACOX1b isoform in a mouse ACOX1b mutant can reverse the hepatic null phenotype, but with only weak reversal of the hepatic steatosis phenotype in the mice, overview. Expression of human isozyme ACOX1a has only poor effects
additional information
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OAF1-gene disrupted construct with reduced number of peroxisomes, no longer inducible by oleate
