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D1819

Sigma-Aldrich

Anti-DYRK1A (C-terminal) antibody produced in rabbit

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-Dual-specificity tyrosine-phosphorylation-regulated kinase 1A, Anti-MNB protein kinase, Anti-MNB/MNBH, Anti-Minibrain Drosophila homolog

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~86 kDa

Espèces réactives

mouse, human, rat

Concentration

~1 mg/mL

Technique(s)

western blot: 1-2 μg/mL using rat brain embryonic extract
western blot: 2-4 μg/mL using rat brain postnatal extract

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... DYRK1A(1859)
mouse ... Dyrk1a(13548)
rat ... Dyrk1a(25255)

Description générale

Dual-specificity tyrosine-phosphorylated regulated kinase 1A (DYRK1A), also known as minibrain/Mnb is a member of a growing family of Ser/Thr protein kinases termed dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs). DYRKs also possess autophosphorylation activity on tyrosine residues, located on the YXY motif of the activation loop of the catalytic domain.
The human and rodent DYRK1A are ubiquitously expressed in adult and fetal tissue with high expression in the brain and heart during development.

Application

Anti-DYRK1A (C-terminal) antibody produced in rabbit has been used in western blotting.

Actions biochimiques/physiologiques

DYRK1A is encoded by a gene located within the Down syndrome (DS) critical region on human chromosome 21 and its expression is found to be elevated in individuals with DS. It might be one of the genes involved in some of the neurological abnormalities observed in DS. It phosphorylates several substrates including transcription factor FKHR, NFAT, STAT3, microtubule-associated protein Tau, glycogen synthase and c-AMP-response element-binding protein.
DYRK1A phosphorylates several substrates including transcription factor FKHR, NFAT, STAT3, microtubule-associated protein Tau, glycogen synthase and c-AMP-response element-binding protein.

Forme physique

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Consulter la Bibliothèque de documents

Emerging Roles of DYRK Kinases in Embryogenesis and Hedgehog Pathway Control
Singh R, et al.
Journal of developmental biology, 5(4) (2017)
DYRK1A-haploinsufficiency in mice causes autistic-like features and febrile seizures
Raveau M, et al.
Neurobiology of Disease, 110, 180-191 (2018)
Noriko Murakami et al.
The Journal of biological chemistry, 281(33), 23712-23724 (2006-05-31)
Minibrain kinase/dual-specificity tyrosine phosphorylation-regulated kinase (Mnb/Dyrk1A) is a proline-directed serine/threonine kinase encoded in the Down syndrome critical region of human chromosome 21. This kinase has been shown to phosphorylate dynamin 1 and synaptojanin 1. Here we report that amphiphysin I
Joseph R Arron et al.
Nature, 441(7093), 595-600 (2006-03-24)
Trisomy 21 results in Down's syndrome, but little is known about how a 1.5-fold increase in gene dosage produces the pleiotropic phenotypes of Down's syndrome. Here we report that two genes, DSCR1 and DYRK1A , lie within the critical region
W J Song et al.
Genomics, 38(3), 331-339 (1996-12-15)
The presence of an extra copy of human chromosome 21 (trisomy 21), especially region 21q22.2, causes many phenotypes in Down syndrome, including mental retardation. To study genes potentially responsible for some of these phenotypes, we cloned a human candidate gene

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