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抗Human DYRK1A 抗体:
抗Mouse (Murine) DYRK1A 抗体:
抗Rat (Rattus) DYRK1A 抗体:
Human Monoclonal DYRK1A Primary Antibody for ELISA, WB - ABIN560675
Aranda, Alvarez, Turró, Laguna, de la Luna: Sprouty2-mediated inhibition of fibroblast growth factor signaling is modulated by the protein kinase DYRK1A. in Molecular and cellular biology 2008
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Human Polyclonal DYRK1A Primary Antibody for WB - ABIN1881275
Park, Oh, Yoo, Jung, Song, Lee, Seo, Chung: Dyrk1A phosphorylates p53 and inhibits proliferation of embryonic neuronal cells. in The Journal of biological chemistry 2010
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Human Polyclonal DYRK1A Primary Antibody for ELISA, WB - ABIN543029
Chang, Lin, Yang, Yen, Lai, Chen, Liang, Yu: Increased expression of Dyrk1a in HPV16 immortalized keratinocytes enable evasion of apoptosis. in International journal of cancer. Journal international du cancer 2007
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Human Polyclonal DYRK1A Primary Antibody for ELISA, WB - ABIN543030
Alvarez, Altafaj, Aranda, de la Luna: DYRK1A autophosphorylation on serine residue 520 modulates its kinase activity via 14-3-3 binding. in Molecular biology of the cell 2007
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DCAF7/WDR68 is required for normal levels of DYRK1A and DYRK1B
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.
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
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.
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.
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.
These results indicate a functional deficiency of DYRK1A as an underlying disease mechanism for autism.
Inhibition of DYRK1A resulted in an increased apoptosis and decrease in invasion and colony formation ability of HNSCC cell lines.
Immunoprecipitation and pulldown experiments identified DCAF7 as an adaptor for the association of the adenovirus E1A protein with DYRK1A and HIPK2
Results associate a decreased level of DYRK1A with Alzheimer's disease and challenge the use of DYRK1A inhibitors in peripheral tissues as treatment.
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.
we suggest that de novo dominant mutations in DYRK1A account for nearly 0.5% of severe developmental disorders due to substantially reduced kinase function
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.
DYRK1A phosphorylation of NFATc1/alphaA at S261, S278, S403 and S409 interfered with NFATc1 ubiquitination and ubiquitin-proteasome degradation.
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.
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.
study uncovered a new regulatory mechanism of DYRK1A degradation by SCF(betaTrCP) in HEK293 cell cycle progression.
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.
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.
mutations in DYRK1A define a syndromic form of autism spectrum disorder and intellectual disability with neurodevelopmental defects consistent with murine and Drosophila knockout models
DYRK1A overexpression induced dramatic deficits in the serotonin contents of the four brain areas tested and major deficits in dopamine and adrenaline contents especially in the hypothalamus.
Increased dosage of DYRK1A, a gene that lies within Hsa21, causes abnormalities in the proliferation and neuronal/astrocytic differentiation of neural progenitor cells in the Down Syndrome embryonic brain.
MEF2D and DYRK1A are coordinately expressed in mouse brain during neurodevelopment. It elucidates a new regulating mechanism of DYRK1A in embryonic brain development and further enriches the evidence of DYRK1A participation in mouse brain neurogenesis.
Our study reveals on the one hand a role of Dyrk1A in ethanol metabolism and on the other hand a deleterious effect of alcohol administration on hepatic Dyrk1A level.
Chronic Dyrk1 inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP and phosphorylated tau pathology.
Normalizing Dyrk1A gene dosage in Ts65Dn mouse rescued the density of senescent cells in cingulate cortex, hippocampus and septum, prevented cholinergic neuron degeneration, and reduced APP expression in hippocampus, Abeta load in cortex and hippocampus, expression of phosphorylated tau at the Ser202 residue in hippocampus and cerebellum, and levels of total tau in the cortex, hippocampus and cerebellum.
Depleting Huntingtin-associated protein 1 (Hap1) promoted the dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)-DDB1 and CUL4 associated factor 7 (Dcaf7) interaction and increased the DYRK1A protein level.
Down-regulation of Dyrk1A returned returned phosphatidylcholine in trisomic cells to original levels.
Taken together, these results strongly suggested that DYRK1A bound to CDKL5 and phosphorylated it on Ser-308, thus interfering with its nuclear localization.
study identifies DYRK1A-STAT as a signaling pathway responsible for the differentiation of neural progenitors into astrocytes, with direct implication for the anomalies in brain development observed in Down syndrome
This study identified decreased neuronal firing rate and deficits in gamma frequency in the prefrontal cortices of transgenic mice overexpressing Dyrk1A.
Increased Dyrk1a gene dosage is a major contributing factor to the abnormal appendicular skeletal phenotype observed in adolescent Ts65Dn Down syndrome mice.
the increased immunostaining of DYRK1A in HIV+ brains without pathology points at dysregulation of DYRK1A as an early event in the neuronal complications of HIV infection.
Our results identify DYRK1A as a physiologically relevant regulator of Treg cell differentiation and suggest a broader role for other DYRK family members in immune homeostasis.
these data suggest that the dosage imbalance of genes other than Dyrk1a is involved in the development of the prenatal bone phenotype in Ts65Dn embryos.
Show the crucial role of the DYRK1A pathway in the regulation of beta cell mass and carbohydrate metabolism in vivo. Activating the DYRK1A pathway could thus represent an innovative way to increase functional beta cell mass.
DYRK1A has a role in lymphopoiesis; Cyclin D3 protein stability is negatively regulated during exit from the proliferative phases of B and T cell development
Dyrk1A has a role in phosphorylation and inactivation of GSK3beta
Study shows that DYRK1A overexpression affects pathways involved in synaptogenesis and synaptic plasticity and influences excitation/inhibition balance toward inhibition
Dyrk1A positively and selectively modulates p120-catenin protein levels, thus having an impact on p120-catenin and Kaiso (and canonical Wnt) gene targets such as siamois and wnt11.
This gene encodes a member of the Dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) family. This member contains a nuclear targeting signal sequence, a protein kinase domain, a leucine zipper motif, and a highly conservative 13-consecutive-histidine repeat. It catalyzes its autophosphorylation on serine/threonine and tyrosine residues. It may play a significant role in a signaling pathway regulating cell proliferation and may be involved in brain development. This gene is a homolog of Drosophila mnb (minibrain) gene and rat Dyrk gene. It is localized in the Down syndrome critical region of chromosome 21, and is considered to be a strong candidate gene for learning defects associated with Down syndrome. Alternative splicing of this gene generates several transcript variants differing from each other either in the 5' UTR or in the 3' coding region. These variants encode at least five different isoforms.
dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A
, dual specificity tyrosine-phosphorylation-regulated kinase 1A
, protein kinase minibrain homolog
, dual specificity tyrosine-phosphorylation-regulated kinase 1A-like
, MNB/DYRK protein kinase
, dual specificity YAK1-related kinase
, mnb protein kinase homolog hp86
, serine/threonine kinase MNB
, serine/threonine-specific protein kinase
, Dual Specificity Yak1-related kinase
, minibrain protein kinase
, Protein kinase minibrain homolog