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DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B
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we found that Dyrk1a strongly affected various aspects of neuronal development, such as dendritic outgrowth, dendritic spine density and cortical migration, during early postnatal development. R205X and E239X, two DYRK1A truncations that were identified in Autism Spectrum Disorders/Intellectual Disability/Developmentally Delayed patients, functioned as loss-of-function mutants.
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that Dyrk1A might promote fibroblast-like synoviocytes proliferation, migration and invasion by suppressing Spry2 expression and activating the ERK MAPK signaling pathway in rheumatoid arthritis
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This study provides evidence for an essential role of DYRK1A as balanced regulator of S-phase entry in Hepatic progenitor cells (HPCs). An exact gene dosage is crucial, as both DYRK1A deficiency and overexpression affect HPC cell cycle progression.
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LncRNA OIP5-AS1 suppressed cell viability, promoted radio-induced apoptosis, and enhanced the radiosensitivity of CRC cells by regulating DYRK1A expression through miR-369-3p.
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The authors show here that chemical inhibition or genetic knockdown of DYRK1A interferes with neural specification of human pluripotent stem cells, a process equating to the earliest stage of human brain development. Specifically, DYRK1A inhibition insulates the self-renewing subpopulation of human pluripotent stem cells from powerful signals that drive neural induction.
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These results indicate a functional deficiency of DYRK1A as an underlying disease mechanism for autism.
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Inhibition of DYRK1A resulted in an increased apoptosis and decrease in invasion and colony formation ability of HNSCC cell lines.
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Immunoprecipitation and pulldown experiments identified DCAF7 as an adaptor for the association of the adenovirus E1A protein with DYRK1A and HIPK2
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Results associate a decreased level of DYRK1A with Alzheimer's disease and challenge the use of DYRK1A inhibitors in peripheral tissues as treatment.
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The locations of disruptive variants (truncating, missense, and splice site mutations), copy number variations, and chromosomal rearrangements affecting DYRK1A functions. DYRK1A is one of the most recurrent genes with disruptive single nucleotide variants implicated in Autism spectrum disorder.
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we suggest that de novo dominant mutations in DYRK1A account for nearly 0.5% of severe developmental disorders due to substantially reduced kinase function
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The data described herein provide the first identification of a DYRK1A-mediated site of phosphorylation on GLI1 within its NLS and may serve as a valuable mechanism for further understanding Hh signaling modulation.
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DYRK1A phosphorylation of NFATc1/alphaA at S261, S278, S403 and S409 interfered with NFATc1 ubiquitination and ubiquitin-proteasome degradation.
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These results suggest that TT genotype derived from SNP rs8126696 of DYRK1A gene is a possible risk factor for sporadic Parkinson disease, especially for males in this Chinese Han population.
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identified the significant associations of the GBA L444P mutation and DYRK1A rs8126696 T allele with the earlier age at onset (AAO) in Parkinson's disease (PD) patients, and the A allele at MS4A6A rs610932 with the delayed AAO of PD.
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study uncovered a new regulatory mechanism of DYRK1A degradation by SCF(betaTrCP) in HEK293 cell cycle progression.
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Identify Dyrk1a as a novel negative regulator of D-cyclin-mediated Rb1/E2f-signalling. As dysregulation of this pathway with impaired cardiomyocyte proliferation leads to cardiomyopathy.
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The deleterious effect of DYRK1A triplication in the formation of the cerebral cortex begins at the onset of neurogenesis, which is relevant to the search for early therapeutic interventions in Down syndrome.
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mutations in DYRK1A define a syndromic form of autism spectrum disorder and intellectual disability with neurodevelopmental defects consistent with murine and Drosophila knockout models
