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54 results for “Dyrk1a”
DATA to support Dyrk1a function in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21)
<p>Four datasets are provided here to support the function of Dyrk1a in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21):</p> <p>- RNAseq data to compare hippocampal expressed genes at postnatal day 30, in the complete inactivation of Dyrk1a in glutamatergic neurons using a Dyrk1a floxed-allele and the Camk2:Cre transgene</p> <p>- data from all the figures</p> <p>-data from all the supplementary figures </p> <p>-data from the quantitative proteomic analysis made from hippocampal extract of wt, Dyrk1a heterozygote, Dp(16)1Yey and Dp(16)1Yey with only two functional copies of Dyrk1a</p> <p>Detailed information are available in the article by Brault et al 2021, deposited in Biorachiv https://doi.org/10.1101/2021.05.01.442242 </p>
DYRK1a inhibitor mediated rescue of Drosophila models of Alzheimer's disease-Down Syndrome phenotypes
<p>Alzheimer's disease (AD) is the most common neurodegenerative disease which is becoming increasingly prevalent due to ageing populations resulting in huge social, economic, and health costs to the community. Despite the pathological processing of genes such as Amyloid Precursor Protein (APP) into Amyloid-b and Microtubule Associated Protein Tau (MAPT) gene, into hyperphosphorylated Tau tangles being known for decades, there remains no treatments to halt disease progression. One population with increased risk of AD are people with Down syndrome (DS), who have a 90% lifetime incidence of AD, due to trisomy of human chromosome 21 (HSA21) resulting in three copies of APP and other AD-associated genes, such as DYRK1A (Dual specificity tyrosine-phosphorylation-regulated kinase 1A) overexpression. This suggests that blocking DYRK1A might have therapeutic potential. However, it is still not clear to what extent DYRK1A overexpression by itself leads to AD-like phenotypes and how these compare to Tau and Amyloid-b mediated pathology. Likewise, it is still not known how effective a DYRK1A antagonist may be at preventing or improving any Tau, Amyloid-b and DYRK1a mediated phenotype. To address these outstanding questions, we characterised Drosophila models with targeted overexpression of human Tau, human Amyloid-b or the fly orthologue of DYRK1A, called minibrain (mnb). We found targeted overexpression of these AD-associated genes caused degeneration of photoreceptor neurons, shortened lifespan, as well as causing loss of locomotor performance, sleep, and memory. Treatment with the experimental DYRK1A inhibitor PST-001 decreased pathological phosphorylation of human Tau (at serine (S) 262). PST-001 reduced degeneration caused by human Tau, Amyloid-b or mnb lengthening lifespan as well as improving locomotion, sleep and memory loss caused by expression of these AD and DS genes. This demonstrated PST-001 effectiveness as a potential new therapeutic targeting AD and DS pathology.</p>
Data from: Sex specific emergence of trisomic Dyrk1a-related skeletal phenotypes in the development of a Down syndrome mouse model
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Data from: Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model
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DYRK1a inhibitor mediated rescue of Drosophila models of Alzheimer’s disease-Down Syndrome phenotypes
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Normalization of dyrk1A and APP Function as an Approach to Improve Cognitive Performance and Decelerate AD Progression in DS Subjects: Epigallocatechin Gallate as Therapeutic Tool
ClinicalTrials.gov study NCT01699711. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Overexpression of Dyrk1A is implicated in several cognitive, electrophysiological and neuromorphological alterations found in a mouse model of Down syndrome
Down syndrome (DS) phenotypes result from the overexpression of several dosage-sensitive genes. The DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A) gene, which has been implicated in the behavioral and neuronal alterations that are characteristic of DS, plays a role in neuronal progenitor proliferation, neuronal differentiation and long-term potentiation (LTP) mechanisms that contribute to the cognitive deficits found in DS. The purpose of this study was to evaluate the effect of Dyrk1A overexpression on the behavioral and cognitive alterations in the Ts65Dn (TS) mouse model, which is the most commonly utilized mouse model of DS, as well as on several neuromorphological and electrophysiological properties proposed to underlie these deficits. In this study, we analyzed the phenotypic differences in the progeny obtained from crosses of TS females and heterozygous Dyrk1A (+/−) male mice. Our results revealed that normalization of the Dyrk1A copy number in TS mice improved working and reference memory based on the Morris water maze and contextual conditioning based on the fear conditioning test and rescued hippocampal LTP. Concomitant with these functional improvements, normalization of the Dyrk1A expression level in TS mice restored the proliferation and differentiation of hippocampal cells in the adult dentate gyrus (DG) and the density of GABAergic and glutamatergic synapse markers in the molecular layer of the hippocampus. However, normalization of the Dyrk1A gene dosage did not affect other structural (e.g., the density of mature hippocampal granule cells, the DG volume and the subgranular zone area) or behavioral (i.e., hyperactivity/attention) alterations found in the TS mouse. These results suggest that Dyrk1A overexpression is involved in some of the cognitive, electrophysiological and neuromorphological alterations, but not in the structural alterations found in DS, and suggest that pharmacological strategies targeting this gene may improve the treatment of DS-associated learning disabilities.
Data from: Overexpression of Dyrk1A is implicated in several cognitive, electrophysiological and neuromorphological alterations found in a mouse model of Down syndrome
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Chromothripsis orchestrates leukemic transformation in blast phase MPN through targetable amplification of DYRK1A [ATAC]
GEO Series GSE240405. Homo sapiens. 14 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
The DYRK1A protein kinase is recruited to a subset of ribosomal protein gene promoters in human and mouse cells [HeLa RNA-seq]
GEO Series GSE158714. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
The DYRK1A protein kinase is recruited to a subset of ribosomal protein gene promoters in human and mouse cells [ChIP-seq]
GEO Series GSE155807. Mus musculus; Homo sapiens. 8 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Kinase-independent activity of DYRK1A promotes viral entry of highly pathogenic human coronaviruses [ATACseq]
GEO Series GSE213997. Chlorocebus sabaeus. 6 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Relieving Dyrk1a repression of MKL1 corrects developmental defects in infantile megakaryocytes
GEO Series GSE204909. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
RNA-sequencing of DYRK1A-deficient (CKO) pre-B and pre-T cells
GEO Series GSE67052. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
Dyrk1a dosage effects on the transcriptome of embryonic hearts from the Dp1Tyb mouse model of Down syndrome using bulk RNAseq
GEO Series GSE196445. Mus musculus. 20 samples. Type: Expression profiling by high throughput sequencing.
Neurodevelopmental disorder risk gene DYRK1A is required for ciliogenesis and brain size in Xenopus embryos
GEO Series GSE149538. Xenopus tropicalis. 6 samples. Type: Expression profiling by high throughput sequencing.
Chromatin-wide profiling of the protein kinase DYRK1A reveals a role as a transcriptional activator of cell growth related genes
GEO Series GSE63712. Homo sapiens. 5 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
The DYRK1A protein kinase is recruited to a subset of ribosomal protein gene promoters in human and mouse cells
GEO Series GSE155809. Mus musculus; Homo sapiens. 20 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Human beta cell proliferation induced by inhibition of Dyrk1a and GSK3b
GEO Series GSE68625. Rattus norvegicus. 170 samples. Type: Expression profiling by high throughput sequencing.
Role of DYRK1A in MPN
GEO Series GSE228060. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
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