Product Pathways - Neuroscience
DYRK1A (D30C10) Rabbit mAb #8765
|W IP||H M R Mk||Endogenous||90||Rabbit IgG|
Reactivity Key: H=Human M=Mouse R=Rat Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
DYRK1A (D30C10) Rabbit mAb recognizes endogenous levels of total DYRK1A protein. This antibody may also recognize a background band at ~65 kDa or ~28 kDa in some cell lines.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn523 of human DYRK1A protein.
The DYRK family includes several dual-specificity tyrosine-phosphorylated and regulated kinases capable of phosphorylating proteins at both Tyr and Ser/Thr residues (1). The DYRK family was identified based on homology to the yeast Yak1 (2) and the Drosophila minibrain (mnb) kinases (3). Seven mammalian isoforms have been discovered, including DYRK1A, DYRK1B, DYRK1C, DYRK2, DYRK3, DYRK4, and DYRK4B. Differences in substrate specificity, expression, and subcellular localization are seen across the DYRK family (4,5). All DYRK proteins have a Tyr-X-Tyr motif in the catalytic domain activation loop; phosphorylation of the second Tyr residue (e.g. Tyr312 of DYRK1A) is necessary for kinase activity. DYRKs typically autophosphorylate the Tyr residue within their activation loop, but phosphorylate substrates at Ser and Thr residues (1,6).
DYRK1A phosphorylates serine and threonine residues within an RPX(S/T)P consensus sequence. Substrates include transcription factors, such as FoxO1 and cAMP response element-binding proteins, such as NFAT (7,8). DYRK1A is ubiquitously expressed in fetal and adult tissues. Transgenic mice with multiple copies of DYRK1A exhibit learning and motor defects, suggesting that it is a dosage-sensitive gene (9). The DYRK1A gene localizes to chromosome 21q22.2, a region implicated by research studies in Down syndrome, and may contribute to pathological traits observed in chromosome 21 trisomy (10).
- Becker, W. and Joost, H.G. (1999) Prog. Nucleic Acid Res. Mol. Biol. 62, 1-17.
- Garrett, S. and Broach, J. (1989) Genes Dev. 3, 1336-1348.
- Tejedor, F. et al. (1995) Neuron 14, 287-301.
- Kentrup, H. et al. (1996) J. Biol. Chem. 271, 3488-3495.
- Becker, W. et al. (1998) J. Biol. Chem. 273, 25893-25902.
- Lochhead, P.A. et al. (2005) Cell 121, 925-936.
- von Groote-Bidlingmaier, F. et al. (2003) Biochem Biophys Res Commun 300, 764-9.
- Gwack, Y. et al. (2006) Nature 441, 646-50.
- Altafaj, X. et al. (2001) Hum Mol Genet 10, 1915-23.
- Guimera, J. et al. (1999) Genomics 57, 407-18.
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For Research Use Only. Not For Use In Diagnostic Procedures.