Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

DYRK2 Antibody #8143

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk (B) (Dg) (Pg) Endogenous 66, 60 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  B=Bovine  Dg=Dog  Pg=Pig
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

DYRK2 Antibody recognizes endogenous levels of total DYRK2 protein. This antibody recognizes both the 66 and 60 kDa splice variants.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly545 of human DYRK2 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using DYRK2 Antibody.

Background

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).

DYRK2 is thought to play a role in checkpoint control of the cell cycle. DYRK2 can phosphorylate p53 at Ser46 following cellular damage, leading to activation of the apoptotic response (7). Overexpression of DYRK2 has also been reported in esophageal and lung adenocarcinomas (8), and its expression levels were shown to be predictive of chemotherapy treatment outcomes in non-small cell lung cancer (9).

  1. Becker, W. and Joost, H.G. (1999) Prog. Nucleic Acid Res. Mol. Biol. 62, 1-17.
  2. Garrett, S. and Broach, J. (1989) Genes Dev. 3, 1336-1348.
  3. Tejedor, F. et al. (1995) Neuron 14, 287-301.
  4. Kentrup, H. et al. (1996) J. Biol. Chem. 271, 3488-3495.
  5. Becker, W. et al. (1998) J. Biol. Chem. 273, 25893-25902.
  6. Lochhead, P.A. et al. (2005) Cell 121, 925-936.
  7. Taira, N. et al. (2007) Mol Cell 25, 725-38.
  8. Miller, C.T. et al. (2003) Cancer Res 63, 4136-43.
  9. Yamashita, S. et al. (2009) Anticancer Res 29, 2753-7.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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