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Merck

AB5403

Sigma-Aldrich

Anti-NMDAR2B Antibody, phosphoTyr 1472

Chemicon®, from rabbit

Synonym(e):

Anti-DEE27, Anti-EIEE27, Anti-GluN2B, Anti-MRD6, Anti-NMDAR2B, Anti-NR2B, Anti-NR3, Anti-hNR3

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About This Item

UNSPSC-Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

Antikörperform

affinity purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Aufgereinigt durch

affinity chromatography

Speziesreaktivität

rat

Hersteller/Markenname

Chemicon®

Methode(n)

western blot: suitable

NCBI-Hinterlegungsnummer

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

Spezifität

NMDAR2B, phosphoTyr1472. The antibody recognizes a protein of ~180 kDa in Western blot. The labeling of the NMDAR2B protein in Western blots of rat brain is blocked by the phosphopeptide but not by the dephosphopeptide. Two additional lower molecular weight bands are present in Western blots of rat brain.

Immunogen

Epitope: phosphoTyr 1472
Synthetic peptide corresponding to amino acids surrounding the phosphoTyr1472 of rat NMDAR2B.

Anwendung

Research Category
Neurowissenschaft
Research Sub Category
Neurotransmitter & Rezeptoren
Anti-NMDAR2B Antibody, phosphoTyr 1472 is an antibody against NMDAR2B for use in WB.
Western blot: 1:1,000

Optimal working dilutions must be determined by the end user.

Physikalische Form

Affinity purified immunoglobulin. Liquid in 10 mM HEPES (pH 7.5), 150 mM NaCl with 100 μg/mL BSA, 50% glycerol and 0.09% sodium azide.

Lagerung und Haltbarkeit

Maintain at -20°C in undiluted for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles. Do not store in a self defrosting freezer.

Rechtliche Hinweise

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

Sofia Lopes et al.
Proceedings of the National Academy of Sciences of the United States of America, 113(26), E3755-E3763 (2016-06-09)
Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer's-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory
Hong-Bin Yang et al.
Journal of neurochemistry, 116(1), 93-104 (2010-11-09)
Selective inhibition of GluN2B-containing NMDA receptor (GluN2BR) in spinal dorsal horn effectively alleviates inflammatory pain, suggesting the up-regulation of GluN2BR function involved in central sensitization. Previous studies have demonstrated that the increase in GluN2BR synaptic expression serves as a key
Sehoon Won et al.
Proceedings of the National Academy of Sciences of the United States of America, 113(32), E4736-E4744 (2016-07-28)
Phosphorylation regulates surface and synaptic expression of NMDA receptors (NMDARs). Both the tyrosine kinase Fyn and the tyrosine phosphatase striatal-enriched protein tyrosine phosphatase (STEP) are known to target the NMDA receptor subunit GluN2B on tyrosine 1472, which is a critical
Jérémy Ferrier et al.
PloS one, 8(10), e77828-e77828 (2013-11-10)
Oxaliplatin is an anticancer drug used for the treatment of advanced colorectal cancer, but it can also cause painful peripheral neuropathies. The pathophysiology of these neuropathies has not been yet fully elucidated, but may involve spinal N-methyl-D-aspartate (NMDA) receptors, particularly
Dan Ren et al.
Neuroscience bulletin, 38(4), 342-358 (2021-12-16)
Central sensitization is essential in maintaining chronic pain induced by chronic pancreatitis (CP), but cortical modulation of painful CP remains elusive. Here, we examined the role of the anterior cingulate cortex (ACC) in the pathogenesis of abdominal hyperalgesia in a

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