Validation Data Gallery
|Sample-dependent, check data in validation data gallery|
19954-1-AP targets GRIN2B in WB, IF,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Full Name||glutamate receptor, ionotropic, N-methyl D-aspartate 2B|
|Calculated molecular weight||166 kDa|
|GenBank accession number||NM_000834|
|Gene ID (NCBI)||2904|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
GRIN2B (also known as GluN2B or NMDAR2B) is a member of the N-methyl-D-aspartate (NMDA) receptor family within the ionotropic glutamate receptor superfamily. NMDA receptors are widely expressed in the central nervous system and play a major role in excitatory synaptic transmission and plasticity (PMID: 23223336). NMDA receptors large multi-subunit complexes arranged into heteromeric assemblies composed of four homologous subunits within a repertoire of over 10 different subunits: eight GluN1 isoforms, four GluN2 subunits (A-D) and two GluN3 subunits (A and B) (PMID: 21395862). Naturally occurring mutations within GRIN2B gene are associated with neurodevelopmental disorders including autism spectrum disorder, attention deficit hyperactivity disorder, epilepsy, and schizophrenia.
Role of astrocytes-derived d-serine in PFOS-induced neurotoxicity through NMDARs in the rat primary hippocampal neurons.
Protective effects of EphB2 on Aβ1-42 oligomer-induced neurotoxicity and synaptic NMDA receptor signaling in hippocampal neurons.
Central nervous system-specific knockout of Brg1 causes growth retardation and neuronal degeneration.
Front Cell Dev Biol
RAB39B Deficiency Impairs Learning and Memory Partially Through Compromising Autophagy.
Front Cell Dev Biol
Profiling of Sexually Dimorphic Genes in Neural Cells to Identify Eif2s3y, Whose Overexpression Causes Autism-Like Behaviors in Male Mice.