Protein Variants | Comment | Organism |
---|---|---|
K188R | site-directed mutagenesis, catalytically inactive mutant | Homo sapiens |
additional information | construction of three deletion mutations of Dyrk1A from C-terminus, including Dyrk1A1-616 without S/T region, Dyrk1A1-588 without His repeats and S/T region, and Dyrk1A1-474 without PEST, His repeats, and S/T region for investigation whether C-terminus of Dyrk1A is responsible for the regulation of tau expression. All three C-terminal deletion mutations of Dyrk1A enhance the expression of tau to a much less extent as compared with the full length Dyrk1A | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
nucleus | Dyrk1A contains a nuclear targeting signal sequence | Homo sapiens | 5634 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q13627 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HEK-293FT cell | - |
Homo sapiens | - |
neuronal cell | - |
Homo sapiens | - |
Subunits | Comment | Organism |
---|---|---|
More | Dyrk1A contains a nuclear targeting signal sequence, a protein kinase domain, a PEST domain (protein domain that is enriched in proline (P), glutamic acid (E), serine (S), and threonine (T) residues), 13 consecutive histidine residues (His repeats) and a serine/threonine rich segment (S/T). The PEST region is located in the C terminus of the catalytic domain. A stretch of 13 histidines located between 607 and 619 amino acid residues follows subsequently a segment of 14 serine/threonine residues | Homo sapiens |
Synonyms | Comment | Organism |
---|---|---|
dual-specificity tyrosine phosphorylation-regulated kinase 1A Dyrk1A | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
physiological function | enzyme Dyrk1A interacts with and phosphorylates diverse cellular proteins including transcription and splicing factors. Dyrk1A enhances tau expression and regulates expression of endogenous tau in neuronal cells, mechanism, overview. Dyrk1A does not enhance tau gene transcription, but increases tau mRNA stability. The enhancement does not require the kinase activity of Dyrk1A, the inactive enzyme mutant K188R also increases tau expression. Dyrk1A increases the expression of tau isoforms containing exon 10 to a larger extent than isoforms lacking exon 10. Dyrk1A is overexpressed in Down syndrome and may play a critical role in the early onset of tau pathology in this disease | Homo sapiens |