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Validated All-in-One™ qPCR Primer for DYRK1A(NM_001396.4) Search again
Product ID:
HQP094970
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DYRK, DYRK1, HP86, MNB, MNBH, MRD7
Gene Description:
dual specificity tyrosine phosphorylation regulated kinase 1A
Target Gene Accession:
NM_001396.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- DYRK1A protein kinase may play a role in regulating the biogenesis of the splicing speckle compartment
- Overexpression of DYRK1A induces multinucleation through overduplication of the centrosome during interphase.
- characterize cyclin L2 as a highly mobile component of nuclear speckles and suggest that DYRK1A may regulate splicing by phosphorylation of cyclin L2
- In this review experimental evidence is compiled and discussed which supports the involvement of MNB/DYRK1A in several neuropathologies and cognitive deficits of Down syndrome.
- Although the function of MNB/DYRK1A in intracellular signalling and regulation of cell function is still poorly defined, current evidence in this review suggests that MNB/DYRK1A kinase may play a role in the regulation of gene expression.
- Neurons were the only cells showing the presence of Mnb kinase in both cell nucleus and cytoplasm. Nuclear localization supports the concept that Mnb may be involved in control of gene expression.
- encodes a serine-threonine kinase but despite its potential involvement in the neurobiological alterations associated with Down syndrome
- DYRK1A may play a critical role in Ras-dependent transducing signals that are required for promoting or maintaining neuronal differentiation
- The present observations indicate modifications in the expression of constitutive Dyrk1A in the cytoplasm and nuclei of neurons in various neurodegenerative diseases associated with tau phosphorylation.
- Mnb/Dyrk1A is responsible for in vivo phosphorylation of amphiphysin I at serine-293.
- There is now compelling evidence that the protein products of two genes on chromosome 21, Down syndrome candidate region 1 (DSCR1) and dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A), interact functionally.
- Our result indicates that DYRK1A could be a key molecule bridging between beta-amyloid production and tau phosphorylation in AD.
- in DS subjects, the brain levels of DYRK1A protein were increased approximately 1.5-fold, indicating that this protein is overexpressed in gene dosage-dependent manner.
- DYRK1A autophosphorylates, via an intramolecular mechanism, on Ser-520, this phosphorylation allows the binding of 14-3-3beta, which in turn stimulates the catalytic activity of DYRK1A
- raised Dyrk1a in HPV16 immortalized keratinocytes and cervical lesions may serve as a candidate antiapoptotic factor in the FKHR regulated pathway and initiate immortalization and tumorigenesis gradually
- DYRK does not require tyrosine phosphorylation for activity in vitro.
- DYRK1A has a role in the hyperphosphorylation of Tau and an extra copy of the DYRK1A gene contributes to the early onset of Alzheimer disease
- Over-expression of DYRK1A in Down syndrome may play a role in accelerating Alzheimer's disease pathogenesis through phosphorylation of beta-amyloid precursor protein (APP).
- Use DYRK1A transgenic mice as a model for partial trisomy 21 and determine changes in brain volume.
- The regulatory effect of E2F1 suggests that DYRK1A may play a role in cell cycle regulation or apoptosis.
- truncating mutations of DYRK1A result in a clinical phenotype including microcephaly.
- Results suggest that DYRK1A increases the transforming potential of HPV16-infected cells because of the greater stability of HPV16E7.
- Dyrk1A-induced tau phosphorylation inhibited its biological activity & promoted self-aggregation. findings suggest novel mechanism by which overexpression of Dyrk1A in Down syndrome brain causes neurofibrillary degeneration via hyperphosphorylation.
- Imbalance of 3R- and 4R-tau in DS brain by Dyrk1A-induced dysregulation of alternative splicing factor-mediated alternative splicing of tau exon 10 represents a novel mechanism of neurofibrillary degeneration
- DYRK1A is involved in nerve degeneration and that overexpression of this kinase may contribute to the early onset of these pathologies in Down syndrome.
- DYRK1A-mediated deregulation of REST is a very early pathological consequence of trisomy 21 with potential to disturb the development of all embryonic lineages.
- Regulation of apoptosis through inhibitory phosphorylation of caspase 9 may play a role in the function of DYRK1A during development and in pathogenesis.
- DYRK1A regulates caspase-9-mediated apoptosis during retina development