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Literature summary for 3.4.17.21 extracted from

  • Thomas, A.G.; Rojas, C.J.; Hill, J.R.; Shaw, M.; Slusher, B.S.
    Bioanalysis of N-acetyl-aspartyl-glutamate as a marker of glutamate carboxypeptidase II inhibition (2010), Anal. Biochem., 404, 94-96.
    View publication on PubMed

Localization

Localization Comment Organism GeneOntology No. Textmining
cell surface of glia and nonmyelinating Schwann cells Homo sapiens 9986
-

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
N-acetyl-L-aspartyl-L-glutamate + H2O Homo sapiens
-
L-glutamate + N-acetyl-L-aspartate
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
brain
-
Homo sapiens
-
cerebrospinal fluid ventricular, lumbar, and subarachnoid Homo sapiens
-
glial cell
-
Homo sapiens
-
nonmyelinating Schwann cell
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
N-acetyl-L-aspartyl-L-glutamate + H2O
-
Homo sapiens L-glutamate + N-acetyl-L-aspartate
-
?

Synonyms

Synonyms Comment Organism
GCP II
-
Homo sapiens

Temperature Optimum [°C]

Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
37
-
assay at, recombinant enzyme Homo sapiens

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
7.7
-
assay at, recombinant enzyme Homo sapiens

General Information

General Information Comment Organism
malfunction inhibition of the GCP II-catalyzed reaction is beneficial for the treatment of degenerative diseases associated with excess glutamate. Inhibition of GCP II is neuroprotective in a variety of cell and animal models of disease involving excess glutamate. N-acetyl-aspartyl-glutamate can acts as a marker of glutamate carboxypeptidase II inhibition Homo sapiens