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Literature summary for 3.5.1.15 extracted from

  • Kumar, S.; Biancotti, J.C.; Matalon, R.; de Vellis, J.
    Lack of aspartoacylase activity disrupts survival and differentiation of neural progenitors and oligodendrocytes in a mouse model of Canavan disease (2009), J. Neurosci. Res., 87, 3415-3427.
    View publication on PubMed
Search for more literature for 3.5.1.15

Protein Variants

Protein Variants Comment Organism
additional information knockout of aspartoacylase activity leads to sponginess and loss of white matter in Canavan disease, and to increased expression/activity of cdk2, NCAM, nestin, vimentin, and NG2. Differentiation of neuronal progenitor cells is arrested, phenotype, overview Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
-
 Mus musculus 5829
-
nucleus
-
 Mus musculus 5634
-

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
brain expression of full-length ASPA at embryonic day 12.5, when oligodendrocyte progenitors first appear during development Mus musculus
-
cerebral white matter
-
 Mus musculus
-
oligodendrocyte ASPA is an oligodendrocyte-specific enzyme, most active in immature oligodendrocytes Mus musculus
-

Synonyms

Synonyms Comment Organism
ASPA
-
 Mus musculus

General Information

General Information Comment Organism
additional information lack of aspartoacylase activity disrupts survival and differentiation of neural progenitors and oligodendrocytes in a mouse model of Canavan disease. ASPA knockout leads to degeneration of white matter Mus musculus