Product Name: DYRK1A (318-324) pY321
Product Number: PE-04BBR00
Size: | 200 µg | | Price: | 30.00 |
| 1 mg | | $US | 60.00 |
Peptide Name: DYRK1A (318-324) pY321
Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases and for epitope mapping of phosphosite-specific antibodies. The peptide sequence is located in the protein kinase catalytic domain activation T loop region between subdomains VII and VIII. Y321 phosphorylation stimulates phosphotransferase activity.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: IYQ-pY-IQS
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Modifications Other: Phosphorylated
Peptide Molecular Mass Calculated: 993 Da
Peptide Purity Percent after Synthesis and Purification: >80
Peptide Appearance: White powder
Peptide Form: Solid
Storage Conditions: -20°C
Storage Stability: stable
Scientific Background: DYRK1A is a protein-serine/threonine kinase of the CMGC group and DYRK family. It is a dual-specificity protein kinase that can phosphorylate tyrosine, serine, and threonine residues, as well as the proteins CRY2, FOXO1, SRSF6 and SIRT1. Phosphorylation at Y321 increases phosphotransferase activity. Phosphorylation at S529 also increases phosphotransferase activity and association with 14-3-3-beta. It is inhibited by RANBP9. It may play a role in cell proliferation pathways such as during brain development. DYRK1A has been found to prolong ERK activation via interactions with RAS, BRAF, and MEK1 and the formation of a RAS/BRAF/MEK1 complex. Overexpression in pheochromocytoma cells potentiated their neuronal differentiation in response to NGF through a RAS/MAPK signalling pathway. DYRK1A may also interact with viral oncoproteins such as adenovirus E1A and HPV-E7. Its role in cancer is unclear: inhibition of caspase-9 by DYRK1A protects mitotic cells from apoptosis, but overexpression attentuated calcineurin signalling, which leads to decreased angiogenesis and tumour growth. Active DYRK1A can induce megakaryocytic tumours (derived from bone marrow cells responsible for producing red blood cells).