Recombinant Human Dual specificity tyrosine-phosphorylation-regulated kinase 1B (DYRK1B MIRK)

1. Dyrk1B was overexpressed in breast cancer tissues and cells and correlates with FoxO1 phosphorylation and cell proliferation. PMID: 28554575
2. High DYRK1B expression is associated with pancreatic and skin cancers. PMID: 26784250
3. The study shows that DYRK1B is a novel ERK2 substrate, uncovering new links between two kinases involved in cell fate decisions. PMID: 26346493
4. Data reveal a novel role for miR-9 in regulation of the NFAT pathway by targeting KPNB1 and DYRK1B. PMID: 25696812
5. NKX3.1 and DYRK1B were shown to interact via the DYRK1B kinase domain. In vitro kinase assay showed that DYRK1B phosphorylated NKX3.1 at serine 185, a residue critical for NKX3.1 steady-state turnover. PMID: 25777618
6. Upregulation of Mirk mRNA expression is mediated by CREB binding to two sites in the Mirk promoter upstream of the transcription start site and one site within exon 4. PMID: 24590896
7. A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in 3 families with metabolic syndrome. PMID: 24827035
8. DYRK1B is a novel Thr(286)-CCND1 kinase that acts independently of GSK3beta to promote CCND1 degradation. PMID: 24134204
9. Mirk/Dyrk1B plays an important role in ovarian cancer cell survival through modulating FoxO translocation. PMID: 22159921
10. In line with a redirection of autocrine toward paracrine HH signaling by a KRAS-DYRK1B network, we find high levels of GLI1 expression restricted to the stromal compartment and not to SHH-expressing tumor cells in pancreatic adenocarcinoma. PMID: 20512148
11. the kinase Mirk is essential for the growth and survival of osteosarcoma cells. PMID: 20042639
12. activation by MKK2 and role as transcriptional activator of HNF1alpha PMID: 11980910
13. p38 MAP Kinase suppresses the function of Mirk as a transcriptional activator only when cells are proliferating PMID: 12384504
14. Mirk is anti-apoptotic in myoblasts PMID: 15851482
15. Mirk is a survival factor for pancreatic ductal adenocarcinoma. Because knockout of Mirk does not cause embryonic lethality, Mirk is not essential for normal cell growth. PMID: 16618736
16. This review summarizes the known regulators and functions of Mirk kinase and outlines opportunities for future studies of Mirk in the fields of muscle and tumor biology. PMID: 16845176
17. GSK-3beta but also DYRK1B modulates cyclin D1 subcellular localization by the phosphorylation of Thr(288). These results suggest that DIF-3 induces degradation of cyclin D1 through the GSK-3beta- and DYRK1B-mediated threonine phosphorylation in HeLa cells PMID: 17046823
18. BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk PMID: 18818203
19. Quiescent pancreatic cancer cells depleted of Mirk became less viable because they were damaged by ROS, and had increased levels of G(1) cyclins to prime cells to escape quiescence. PMID: 19351855
20. Mirk, through regulating cyclin D turnover, and the CDK inhibitor p27, as shown by depletion studies, functioned independently and additively to regulate the exit of tumor cells from quiescence. PMID: 19542220

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HGNC: 3092

OMIM: 604556

KEGG: hsa:9149

STRING: 9606.ENSP00000312789

UniGene: Hs.130988