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Literature summary for 2.7.12.1 extracted from

  • Liu, F.; Liang, Z.; Wegiel, J.; Hwang, Y.W.; Iqbal, K.; Grundke-Iqbal, I.; Ramakrishna, N.; Gong, C.X.
    Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome (2008), FASEB J., 22, 3224-3233.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.12.1

Application

Application Comment Organism
medicine molecular mechanism by which neurofibrillary degeneration occurs in adults with Down syndrome Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
cytoplasm
-
 Homo sapiens 5737
-
nucleus
-
 Homo sapiens 5634
-

Organism

Organism UniProt Comment Textmining
Homo sapiens Q13627 adult patients with Down syndrome
-

Purification (Commentary)

Purification (Comment) Organism
gel filtration Homo sapiens

Source Tissue

Source Tissue Comment Organism Textmining
brain
-
 Homo sapiens
-
neuron
-
 Homo sapiens
-

Specific Activity [micromol/min/mg]

Specific Activity Minimum [µmol/min/mg] Specific Activity Maximum [µmol/min/mg] Comment Organism
additional information
-
 presence of an extra copy of the Dyrk1A gene due to trisomy 21 results in overexpression of Dyrk1A and elevated kinase activity in brain of Down syndrome patients, tau phosphorylation, enzyme kinetics, and Dyrk1A kinase assays, nuclear and cytoplasmic Dyrk1A may contribute to Down syndrome via different mechanisms Homo sapiens

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information participation in regulating tau phosphorylation, provides a novel mechanism leading to neurofibrillary pathology in Down syndrome Homo sapiens ?
-
 ?

Synonyms

Synonyms Comment Organism
DYRK1A
-
 Homo sapiens