anti-Dual-Specificity tyrosine-(Y)-phosphorylation Regulated Kinase 1B (DYRK1B) Antibodies

Human Dual-Specificity tyrosine-(Y)-phosphorylation Regulated Kinase 1B (DYRK1B) interaction partners

1. DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B

2. DYRK1B mutations associated with metabolic syndrome interfere with the maturation of DYRK1B by tyrosine autophosphorylation and compromise the conformational stability of the catalytic domain, which renders the kinase susceptible to misfolding.

3. Through the activation of DYRK1B, Hedgehog signaling facilitates microtubule-dependent processes such as intracellular mitochondrial transport, mesenchymal cell polarization or directed cell migration.

4. Dyrk1B was overexpressed in breast cancer tissues and cells and correlates with FoxO1 phosphorylation and cell proliferation.

5. High DYRK1B expression is associated with pancreatic and skin cancers.

6. The study shows that DYRK1B is a novel ERK2 substrate, uncovering new links between two kinases involved in cell fate decisions.

7. Data reveal a novel role for miR-9 in regulation of the NFAT pathway by targeting KPNB1 and DYRK1B.

8. 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.

9. 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.

10. A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in 3 families with metabolic syndrome.

11. DYRK1B is a novel Thr(286)-CCND1 kinase that acts independently of GSK3beta to promote CCND1 degradation.

12. Mirk/Dyrk1B plays an important role in ovarian cancer cell survival through modulating FoxO translocation.

13. 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.

14. the kinase Mirk is essential for the growth and survival of osteosarcoma cells.

15. activation by MKK2 and role as transcriptional activator of HNF1alpha

16. p38 MAP Kinase suppresses the function of Mirk as a transcriptional activator only when cells are proliferating

17. Mirk is anti-apoptotic in myoblasts

18. 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.

19. 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.

20. 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

Mouse (Murine) Dual-Specificity tyrosine-(Y)-phosphorylation Regulated Kinase 1B (DYRK1B) interaction partners

1. we demonstrated that Anxa1, Anxa2, and Dyrk1b are upregulated at both the transcriptional and translational levels by the overexpression of GAS1

2. Through the activation of DYRK1B, Hedgehog signaling facilitates microtubule-dependent processes such as intracellular mitochondrial transport, mesenchymal cell polarization or directed cell migration.

3. results suggest that functional interactions between BM88/Cend1, RanBPM and Dyrk1B affect the balance between cellular proliferation and differentiation in Neuro 2a cells

4. Cirp functions to fine-tune the proliferation of undifferentiated spermatogonia by interacting with Dyrk1b.

5. p38 MAP Kinase suppresses the function of Mirk as a transcriptional activator only when cells are proliferating

6. dyrk1B is a Rho-induced kinase active in skeletal muscle differentiation

7. p27Kip1 is stabilized in G(0) by Mirk/dyrk1B kinase

8. Mirk may function together with GSK3beta to assist cell arrest by destabilizing cyclin D1.

9. Mirk is induced within the initial 24 h of myogenic differentiation and enables MEF2 to transcribe the myogenin gene by decreasing the nuclear accumulation of class II HDACs

10. Mirk is anti-apoptotic in myoblasts

11. BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk