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Description

Glutamate receptor ionotropic, NMDA2B (UniProt: Q13224, also known GluN2B, Glutamate [NMDA] receptor subunit epsilon-2, N-methyl D-aspartate receptor subtype 2B, NMDAR2B, NR2B, N-methyl-D-aspartate receptor subunit 3, NR3, hNR3) is encoded by the GRIN2B (also known as NMDAR2B) gene (Gene ID: 2904) in human. NMDA receptor complexes are ligand-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. They are involved in long-term potentiation and neuronal plasticity and regulate the number of nerve cells during development. However, over-stimulation NMDA receptors can lead to neuronal degeneration. NMDAR2B is a heterotetrameric, multi-pass membrane protein that is synthesized with a signal peptide (aa 1-26), which is subsequently cleaved off in the mature form. The heterotetrameric channel is composed of two zeta subunits and two epsilon subunits, but can also form channels that contain at least one zeta subunit and at least one epsilon subunit. Activation of NMDA 2B channel requires binding of glutamate to the epsilon subunit, glycine binding to the zeta subunit, plus membrane depolarization to eliminate channel inhibition by magnesium ions. NMDA 2B is reported to be phosphorylated at Ser1303 by DAPK1 that enhances its channel activity allowing injurious Ca2+ influx that results in neuronal death. Mutations in NMDAR2B have been linked to early infantile epileptic encephalopathy that is characterized by refractory seizures and neurodevelopmental impairment. Some mutations are also known to cause mental retardation with or without seizures.