Anti-NMDAR2A antibody [S327-95] - N-terminal,Abcam,AB240884
Host
Mouse
Reactivity
Human
Application
ICC/IF, WB
Platform ID
BAB715457089

Abcam
Contact
Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215
Email:
Specifications
Scientific Background
Target data Component of N-methyl-D-aspartate (NMDA) receptors (NMDARs) that function as heterotetrameric, ligand-gated cation channels with high calcium permeability and voltage-dependent block by Mg(2+) (PubMed : 20890276, PubMed : 23933818, PubMed : 23933819, PubMed : 23933820, PubMed : 24504326, PubMed : 26875626, PubMed : 26919761, PubMed : 28242877, PubMed : 36117210, PubMed : 38538865, PubMed : 8768735). NMDARs participate in synaptic plasticity for learning and memory formation by contributing to the slow phase of excitatory postsynaptic current, long-term synaptic potentiation, and learning (By similarity). Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+) (PubMed : 23933818, PubMed : 23933819, PubMed : 23933820, PubMed : 24504326, PubMed : 26875626, PubMed : 26919761, PubMed : 27288002, PubMed : 28095420, PubMed : 28105280, PubMed : 28126851, PubMed : 28182669, PubMed : 29644724, PubMed : 38307912, PubMed : 8768735). NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators (PubMed : 26875626, PubMed : 26919761). Participates in the synaptic plasticity regulation through activation by the L-glutamate releaseed by BEST1, into the synaptic cleft, upon F2R/PAR-1 activation in astrocyte (By similarity). See full target information GRIN2A
Category Paths
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