Home > Product > Antibody > Rabbit Anti-Phospho-NMDAR2B (Tyr1474)/FITC Conjugated antibody
NMDAR2B (Phospho-Tyr1474); NMDAR2B (Phospho-Y1474); p-NMDAR2B (Tyr1474); p-NMDAR2B (Y1474); AW490526; Glutamate [NMDA] receptor subunit epsilon 2; Glutamate [NMDA] receptor subunit epsilon-2; Glutamate Receptor Ionotropic N Methyl D Aspartate 2B; Glutamat
Cat:
SL8566R-FITC
Species Reactivity:
Human,(predicted: Mouse,Rat,Chicken,Dog,Pig,Cow,Horse,)
Immunogen:
KLH conjugated synthesised phosphopeptide derived from human NMDAR2B around the phosphorylation site of Tyr1474
Format:
Lyophilized or Liquid
Storage instructions:
Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of ant
Buffer:
0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Concentration:
1mg/ml
Clonality:
Polyclonal
Isotype:
IgG
Applications:
ICC=1:50-200IF=1:50-200not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.
Host:
Rabbit
Calculated MW:
163kDa
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Unit:
Price: $
Product PDFs
Datasheet:


background:
N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate receptors. NMDA receptor channel has been shown to be involved in long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning. NMDA receptor channels are heteromers composed of three different subunits: NR1 (GRIN1), NR2 (GRIN2A, GRIN2B, GRIN2C, or GRIN2D) and NR3 (GRIN3A or GRIN3B). The NR2 subunit acts as the agonist binding site for glutamate. This receptor is the predominant excitatory neurotransmitter receptor in the mammalian brain. [provided by RefSeq, Jul 2008].

Function:
NMDA receptor subtype of glutamate-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death.

Subunit:
Forms heteromeric channel of a zeta subunit (GRIN1), a epsilon subunit (GRIN2A, GRIN2B, GRIN2C or GRIN2D) and a third subunit (GRIN3A or GRIN3B). Found in a complex with GRIN1 and GRIN3B. Found in a complex with GRIN1, GRIN3A and PPP2CB. Interacts with PDZ domains of INADL and DLG4. Interacts with HIP1 and NETO1. Interacts with MAGI3. Interacts with DAPK1.

Subcellular Location:
Cell membrane; Multi-pass membrane protein. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein.

Tissue Specificity:
Primarily found in the fronto-parieto-temporal cortex and hippocampus pyramidal cells, lower expression in the basal ganglia.

Post-translational modifications:
Phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity.

DISEASE:
Defects in GRIN2B are the cause of mental retardation autosomal dominant type 6 (MRD6) [MIM:613970]. Mental retardation is characterized by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. Note=Chromosomal aberrations involving GRIN2B have been found in patients with mental retardation. Translocations t(9;12)(p23;p13.1) and t(10;12)(q21.1;p13.1) with a common breakpoint in 12p13.1.

Similarity:
Belongs to the glutamate-gated ion channel (TC 1.A.10.1) family. NR2B/GRIN2B subfamily.

Database links:

Entrez Gene: 2904 Human

Entrez Gene: 14812 Mouse

Entrez Gene: 24410 Rat

Omim: 138252 Human

SwissProt: Q13224 Human

SwissProt: Q01097 Mouse

SwissProt: Q00960 Rat

Unigene: 654430 Human

Unigene: 436649 Mouse

Unigene: 9711 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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