| Pathogenic, Total Loss-of-Function DYRK1B Variants Cause Monogenic Obesity Associated With Type 2 Diabetes. | Pathogenic, Total Loss-of-Function DYRK1B Variants Cause Monogenic Obesity Associated With Type 2 Diabetes.
Folon L, Baron M, Scherrer V, Toussaint B, Vaillant E, Loiselle H, Dechaume A, De Pooter F, Boutry R, Boissel M, Diallo A, Ning L, Balkau B, Charpentier G, Franc S, Marre M, Derhourhi M, Froguel P, Bonnefond A. | 02/26/2024 |
| Targeting the survival kinase DYRK1B: A novel approach to overcome radiotherapy-related treatment resistance. | Targeting the survival kinase DYRK1B: A novel approach to overcome radiotherapy-related treatment resistance.
Beckers C, Vasilikos L, Sanchez Fernandez A, Moor L, Pruschy M. | 02/22/2024 |
| Analysis of DYRK1B, PPARG, and CEBPB Expression Patterns in Adipose-Derived Stem Cells from Patients Carrying DYRK1B R102C and Healthy Individuals During Adipogenesis. | Analysis of DYRK1B, PPARG, and CEBPB Expression Patterns in Adipose-Derived Stem Cells from Patients Carrying DYRK1B R102C and Healthy Individuals During Adipogenesis.
Armanmehr A, Jafari Khamirani H, Zoghi S, Dianatpour M. | 12/31/2022 |
| DYRK1B-STAT3 Drives Cardiac Hypertrophy and Heart Failure by Impairing Mitochondrial Bioenergetics. | DYRK1B-STAT3 Drives Cardiac Hypertrophy and Heart Failure by Impairing Mitochondrial Bioenergetics.
Zhuang L, Jia K, Chen C, Li Z, Zhao J, Hu J, Zhang H, Fan Q, Huang C, Xie H, Lu L, Shen W, Ning G, Wang J, Zhang R, Chen K, Yan X. | 04/23/2022 |
| Differential maturation and chaperone dependence of the paralogous protein kinases DYRK1A and DYRK1B. | Differential maturation and chaperone dependence of the paralogous protein kinases DYRK1A and DYRK1B.
Papenfuss M, Lützow S, Wilms G, Babendreyer A, Flaßhoff M, Kunick C, Becker W., Free PMC Article | 03/19/2022 |
| Suppression of DYRK1A/B Drives Endoplasmic Reticulum Stress-mediated Autophagic Cell Death Through Metabolic Reprogramming in Colorectal Cancer Cells. | Suppression of DYRK1A/B Drives Endoplasmic Reticulum Stress-mediated Autophagic Cell Death Through Metabolic Reprogramming in Colorectal Cancer Cells.
Hwang J, Park A, Kim C, Yu D, Byun H, Ku M, Yang J, Kim TI, Jeong KS, Kim KY, Lee H, Shin SJ. | 01/15/2022 |
| Study of DYRK1B gene expression and its association with metabolic syndrome in a small cohort of Egyptians. | Study of DYRK1B gene expression and its association with metabolic syndrome in a small cohort of Egyptians.
Mohamed YA, Hassaneen HM, El-Dessouky MA, Safwat G, Hassan NA, Amr K. | 01/8/2022 |
| Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin. | Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin.
Dong C, West KL, Tan XY, Li J, Ishibashi T, Yu CH, Sy SMH, Leung JWC, Huen MSY., Free PMC Article | 09/19/2020 |
| Proline Hydroxylation Primes Protein Kinases for Autophosphorylation and Activation. | Proline Hydroxylation Primes Protein Kinases for Autophosphorylation and Activation.
Lee SB, Ko A, Oh YT, Shi P, D'Angelo F, Frangaj B, Koller A, Chen EI, Cardozo T, Iavarone A, Lasorella A., Free PMC Article | 08/29/2020 |
| Human cytomegalovirus(HCMV) modulates cellular dual specificity tyrosine phosphorylation regulated kinase 1B (DYRK1B) during placental replication which may have implications for congenital HCMV pathogenesis and represent promising antiviral targets. | Human cytomegalovirus utilises cellular dual-specificity tyrosine phosphorylation-regulated kinases during placental replication.
Hamilton ST, Hutterer C, Egilmezer E, Steingruber M, Milbradt J, Marschall M, Rawlinson WD. | 09/21/2019 |
| DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B | DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B.
Yousefelahiyeh M, Xu J, Alvarado E, Yu Y, Salven D, Nissen RM., Free PMC Article | 04/27/2019 |
| 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. | DYRK1B mutations associated with metabolic syndrome impair the chaperone-dependent maturation of the kinase domain.
Abu Jhaisha S, Widowati EW, Kii I, Sonamoto R, Knapp S, Papadopoulos C, Becker W., Free PMC Article | 03/9/2019 |
| Through the activation of DYRK1B, Hedgehog signaling facilitates microtubule-dependent processes such as intracellular mitochondrial transport, mesenchymal cell polarization or directed cell migration. | DYRK1B regulates Hedgehog-induced microtubule acetylation.
Singh R, Holz PS, Roth K, Hupfer A, Meissner W, Müller R, Buchholz M, Gress TM, Elsässer HP, Jacob R, Lauth M., Free PMC Article | 01/26/2019 |
| Dyrk1B was overexpressed in breast cancer tissues and cells and correlates with FoxO1 phosphorylation and cell proliferation. | Dyrk1B overexpression is associated with breast cancer growth and a poor prognosis.
Chen Y, Wang S, He Z, Sun F, Huang Y, Ni Q, Wang H, Wang Y, Cheng C. | 10/7/2017 |
| High DYRK1B expression is associated with pancreatic and skin cancers. | DYRK1B as therapeutic target in Hedgehog/GLI-dependent cancer cells with Smoothened inhibitor resistance.
Gruber W, Hutzinger M, Elmer DP, Parigger T, Sternberg C, Cegielkowski L, Zaja M, Leban J, Michel S, Hamm S, Vitt D, Aberger F., Free PMC Article | 12/24/2016 |
| The study shows that DYRK1B is a novel ERK2 substrate, uncovering new links between two kinases involved in cell fate decisions. | Identification of DYRK1B as a substrate of ERK1/2 and characterisation of the kinase activity of DYRK1B mutants from cancer and metabolic syndrome.
Ashford AL, Dunkley TP, Cockerill M, Rowlinson RA, Baak LM, Gallo R, Balmanno K, Goodwin LM, Ward RA, Lochhead PA, Guichard S, Hudson K, Cook SJ., Free PMC Article | 06/28/2016 |
| Data reveal a novel role for miR-9 in regulation of the NFAT pathway by targeting KPNB1 and DYRK1B. | miR-9 enhances the transactivation of nuclear factor of activated T cells by targeting KPNB1 and DYRK1B.
Zeng Y, Wang Y, Wu Z, Kang K, Peng X, Peng W, Qu J, Liu L, Raj JU, Gou D. | 03/19/2016 |
| 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. | The Tumor Suppressor NKX3.1 Is Targeted for Degradation by DYRK1B Kinase.
Song LN, Silva J, Koller A, Rosenthal A, Chen EI, Gelmann EP., Free PMC Article | 03/12/2016 |
| 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. | Mirk/dyrk1B kinase is upregulated following inhibition of mTOR.
Deng X, Hu J, Ewton DZ, Friedman E., Free PMC Article | 10/25/2014 |
| A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in 3 families with metabolic syndrome. | A form of the metabolic syndrome associated with mutations in DYRK1B.
Keramati AR, Fathzadeh M, Go GW, Singh R, Choi M, Faramarzi S, Mane S, Kasaei M, Sarajzadeh-Fard K, Hwa J, Kidd KK, Babaee Bigi MA, Malekzadeh R, Hosseinian A, Babaei M, Lifton RP, Mani A., Free PMC Article | 06/7/2014 |
| DYRK1B is a novel Thr(286)-CCND1 kinase that acts independently of GSK3beta to promote CCND1 degradation. | A novel DYRK1B inhibitor AZ191 demonstrates that DYRK1B acts independently of GSK3β to phosphorylate cyclin D1 at Thr(286), not Thr(288).
Ashford AL, Oxley D, Kettle J, Hudson K, Guichard S, Cook SJ, Lochhead PA. | 03/8/2014 |
| Mirk/Dyrk1B plays an important role in ovarian cancer cell survival through modulating FoxO translocation. | The involvement of FoxO in cell survival and chemosensitivity mediated by Mirk/Dyrk1B in ovarian cancer.
Gao J, Yang X, Yin P, Hu W, Liao H, Miao Z, Pan C, Li N., Free PMC Article | 09/1/2012 |
| 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. | DYRK1B-dependent autocrine-to-paracrine shift of Hedgehog signaling by mutant RAS.
Lauth M, Bergström A, Shimokawa T, Tostar U, Jin Q, Fendrich V, Guerra C, Barbacid M, Toftgård R. | 06/28/2010 |
| the kinase Mirk is essential for the growth and survival of osteosarcoma cells. | The kinase Mirk is a potential therapeutic target in osteosarcoma.
Yang C, Ji D, Weinstein EJ, Choy E, Hornicek FJ, Wood KB, Liu X, Mankin H, Duan Z., Free PMC Article | 04/19/2010 |
| 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. | Mirk regulates the exit of colon cancer cells from quiescence.
Jin K, Ewton DZ, Park S, Hu J, Friedman E., Free PMC Article | 01/21/2010 |