An antibody raised against dual specificity tyrosine-phosphorylation-regulated kinase 3 (DYRK3); a dual-specificity protein kinase that promotes the disassembly of several types of membrane-less organelles during mitosis.
Catalogue number crb2005740 Antibody Anti-DYRK3 antibody Antigen Peptide KLH conjugated synthetic peptide crb1200949 Protein ID UniProtKB - O43781 Aliases Dual specificity tyrosine-phosphorylation-regulated kinase 3, Regulatory erythroid kinase (REDK) Cross-Reactivity Human Host Species Rabbit Antibody Type Polyclonal Concentration 2.0 mg/ml Glycine Target DYRK3 Family CMGC Ser/Thr protein kinase family Super Family Protein kinase superfamily Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References
Kim et al., (2021). Dual specificity kinase DYRK3 promotes aggressiveness of glioblastoma by altering mitochondrial morphology and function. International Journal of Molecular Sciences, 22(6): 2982. doi: 10.3390/ijms22062982.
Mediani et al., (2021). Hsp90‐mediated regulation of DYRK3 couples stress granule disassembly and growth via mTORC1 signaling. EMBO reports, 22(5): e51740. doi: 10.15252/embr.202051740.
Wippich et al., (2013). Dual specificity kinase DYRK3 couples stress granule condensation/dissolution to mTORC1 signaling. Cell, 152(4): 791. doi: 10.1016/j.cell.2013.01.033.
Dual specificity tyrosine-phosphorylation-regulated kinase 3 (DYRK3) acts as a central dissolvase of membraneless organelles during the G2-to-M transition. DYRK3 mediates the phosphorylation of multiple serine and threonine residues in unstructured domains of proteins, including SRRM1 and PCM1.
DYRK3 is a key regulator of mTORC1 by mediating the dissolution of stress granules. During stressful conditions, DYRK3 partitions from the cytosol to the stress granule with mTORC1 components, which prevents mTORC1 signalling. When homeostasis is achieved, the kinase activity of DYRK3 is required for the dissolution of stress granule and mTORC1 relocation to the cytosol. DYRK3 mediates phosphorylation of signalling mTORC1 via inhibitor AKT1S1, allowing full reactivation of mTORC1 signalling.
DYRK3 is a negative regulator of EPO-dependent erythropoiesis and may place an upper limit on red cell production during stress erythropoiesis. DYRK3 also inhibits cell death due to cytokine withdrawal in hematopoietic progenitor cells.
Overexpression of DYRK3 has been linked to glioblastoma multiforme (GBM) and can be a strong predictive factor of a patient’s survival chances.