3.5.1.15: aspartoacylase
This is an abbreviated version!
For detailed information about aspartoacylase, go to the full flat file.
Word Map on EC 3.5.1.15
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3.5.1.15
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canavan
-
n-acetylaspartate
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leukodystrophy
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matter
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myelin
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oligodendrocyte
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spongy
-
n-acetyl-l-aspartate
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spongiform
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macrocephaly
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tremor
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ashkenazi
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jewish
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non-jewish
-
dysmyelination
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nutrition
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medicine
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pharmacology
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n-acetylaspartylglutamate
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triacetate
- 3.5.1.15
- canavan
- n-acetylaspartate
- leukodystrophy
- matter
- myelin
- oligodendrocyte
-
spongy
- n-acetyl-l-aspartate
-
spongiform
- macrocephaly
- tremor
-
ashkenazi
-
jewish
-
non-jewish
-
dysmyelination
- nutrition
- medicine
- pharmacology
- n-acetylaspartylglutamate
- triacetate
Reaction
Synonyms
acetyl-aspartic deaminase, Acylase II, aminoacylase 2, Aminoacylase II, aminoacylase-2, ASPA, aspartic acid acylase, Aspartoacylase, aspartoacylase II, hASPA, human ASPA, More, murine aspartoacylase, N-acetyl-aspartate deacetylase, N-Acetyl-L-aspartate amidohydrolase, N-Acetylaspartate amidohydrolase, N-acetylaspartocylase, NAA acylase
ECTree
3.5.1.15 aspartoacylaseAdvanced search results
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results (Substrates Products
Substrates Products on EC 3.5.1.15 - aspartoacylase
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SUBSTRATE 
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
chloroacetyl-L-asparagine + H2O
chloroacetate + L-asparagine
-
poor substrate
-
-
?
N-acetylalanine + H2O
acetate + alanine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylarginine + H2O
acetate + arginine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylaspartate + H2O
L-aspartate + acetate
-
aspartocylase deficiency results in elevated levels of substrate, brain edema and dysmyelination
-
-
?
N-acetylcysteine + H2O
acetate + cysteine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylglutamate + H2O
acetate + glutamate
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylglutamine + H2O
acetate + glutamine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylleucine + H2O
acetate + leucine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetyllysine + H2O
acetate + lysine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylmethionine + H2O
acetate + methionine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylphenylalanine + H2O
acetate + phenylalanine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetylproline + H2O
acetate + proline
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-acetyltyrosine + H2O
acetate + tyrosine
poor substrate, 0.1% of the activity towards N-acetyl-aspartate
-
-
?
N-trifluoroacetyl-L-aspartate + H2O
trifluoroacetate + L-aspartate
-
-
-
?
N-acetyl-L-aspartate + H2O
acetate + L-aspartate
aspartoacylase is a key enzyme in the human central nervous system. N-Acetyl-L-aspartate is a precursor for the synthesis of the dipeptide N-acetylaspartyl-glutamate, which participates in the neuromodulation of metabotropic and NMDA receptors (NMDA is N-methyl-D-aspartate), regulates the intracellular pressure in neurons and is involved in the energy generation from glutamate anions in neuronal mitochondria. N-Acetyl-L-aspartate is a source of acetyl groups for the construction of myelin sheath in the brain. Therefore, maintenance of the N-acetyl-L-aspartate level ensures proper development and functions of white matter
-
-
?
N-acetyl-L-aspartate + H2O
acetate + L-aspartate
the enzyme hydrolyzes one of the most abundant amino acid derivatives in the brain, N-acetyl-aspartate
-
-
?
N-acetyl-L-aspartate + H2O
aspartate + acetate
enzyme mutations cause the Canavan disease
-
-
?
N-acetyl-L-aspartate + H2O
aspartate + acetate
deficiency in enzyme activity leads to spongiform degeneration of the white matter of the brain and is the established cause of Canavan disease
-
-
?
N-acetyl-L-aspartate + H2O
aspartate + acetate
-
deficiency in enzyme activity leads to spongiform degeneration of the white matter of the brain and is the established cause of Canavan disease
-
-
?
N-acetyl-L-aspartate + H2O
L-aspartate + acetate
malfunction of the enzyme causes Canavan disease
-
-
?
N-acetyl-L-aspartic acid + H2O
acetate + aspartic acid
-
-
-
-
?
N-acetyl-L-aspartic acid + H2O
acetate + aspartic acid
-
-
-
-
?
N-acetyl-L-aspartic acid + H2O
acetate + aspartic acid
-
-
-
-
?
N-acetyl-L-aspartic acid + H2O
acetate + aspartic acid
-
-
-
-
?
N-acetylasparagine + H2O
acetate + aspartate + NH3
-
10% of the activity towards N-acetylaspartate
product is aspartate, not asparagine, indicating the enzyme catalyzes deacetylation as well as hydrolysis of the beta acid amide
?
N-acetylasparagine + H2O
acetate + aspartate + NH3
10% of the activity towards N-acetylaspartate
product is aspartate, not asparagine, indicating the enzyme catalyzes deacetylation as well as hydrolysis of the beta acid amide
?
N-acetylaspartic acid + H2O
aspartate + acetate
-
enzyme mutations cause the Canavan disease and type 2 diabetes
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
enzyme deficiency causes the Canavan disease, an autosomal-recessive neurodegenerative disorder
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
enzyme mutations cause the Canavan disease
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
enzyme deficiency, due to mutations of aspartoacylase II, causes the Canavan disease, which is associated with optical neuropathy
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
hydrolysis of N-acetylaspartic acid is important to maintain healthy neurons, the enzyme is upregulated in duodenum of obesity-induced diabetic mice, which might be responsible for diabetic neuropathy, overview
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
-
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
enzyme mutations cause the Canavan disease
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
-
restoration of deficient enzyme activity by enzyme expression in CNS neurons does not ameliorate motor deficits and demyelination in a model of Canavan disease, which is caused by elevated levels of N-acetylaspartic acid, NAA, neuronal expression of ASPA can compensate for NAA-mediated neuronal hyperexcitation, but not for oligodebdrocyte dysfunciton, overview
-
-
?
N-acetylaspartic acid + H2O
L-asparatate + acetate
the enzyme is involved in negative regulation of brain-derived neurotrophic factor, BDNF, and timing of postnatal oligodendrogenesis, overview
-
-
?
N-acyl L-aspartic acid + H2O
acetate + L-aspartate
-
-
-
-
?
N-acyl L-aspartic acid + H2O
acetate + L-aspartate
-
-
-
-
?
N-acyl L-aspartic acid + H2O
acetate + L-aspartate
-
-
-
-
?
N-acyl L-aspartic acid + H2O
acetate + L-aspartate
-
-
-
-
?
additional information
?
-
-
the enzyme functions in concert with the plasma membrane transporter NaDC3, that specifically transports N-acetylaspartic acid into the cell
-
-
?
additional information
?
-
-
N-methyl aspartic acid, N-carbamoyl aspartic acid and N-glycyl aspartic acids are no substrates
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-
?
