D1819
Anti-DYRK1A (C-terminal) antibody produced in rabbit
~1 mg/mL, affinity isolated antibody, buffered aqueous solution
别名:
Anti-Dual-specificity tyrosine-phosphorylation-regulated kinase 1A, Anti-MNB protein kinase, Anti-MNB/MNBH, Anti-Minibrain Drosophila homolog
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关于此项目
NACRES:
NA.41
UNSPSC Code:
12352203
Conjugate:
unconjugated
Clone:
polyclonal
Application:
WB
Citations:
9
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~86 kDa
species reactivity
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
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... DYRK1A(1859)
mouse ... Dyrk1a(13548)
rat ... Dyrk1a(25255)
General description
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.
Biochem/physiol Actions
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.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
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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存储类别
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves
法规信息
常规特殊物品
此项目有
DYRK1A-haploinsufficiency in mice causes autistic-like features and febrile seizures
Raveau M, et al.
Neurobiology of Disease, 110, 180-191 (2018)
Emerging Roles of DYRK Kinases in Embryogenesis and Hedgehog Pathway Control
Singh R, et al.
Journal of developmental biology, 5(4) (2017)
Rodolphe Dard et al.
Genes, 12(11) (2021-11-28)
Down syndrome (DS) is the most common chromosomal disorder. It is responsible for intellectual disability (ID) and several medical conditions. Although men with DS are thought to be infertile, some spontaneous paternities have been reported. The few studies of the
Hada Buhe et al.
Acta pharmacologica Sinica (2022-12-15)
Neoplastic cells of non-immunogenic pancreatic ductal adenocarcinoma (PDAC) express indoleamine 2,3-dioxygenase 1 (IDO-1), an immunosuppressive enzyme. The metabolites of IDO-1 in cancers provide one-carbon units that annihilate effector T cells, and recruit immunosuppressive cells. In this study we investigated how
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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