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In vitro DNA-binding and reporter gene assays of different allele combinations in transfected cells showed that the A allele was a gain-of-function variant associated with increasing GRIN2B mRNA levels
Polymorphism C366G of gene GRIN2B and verbal episodic memory: No association with schizophrenia
These results indicate these individuals may have suffered neurodevelopmental deficits as a result of the decreased presence of GluN1 (show GRIN1 Proteins)-G620R/GluN2B complexes on the neuronal surface during embryonic brain development and reduced current responses of GluN1 (show GRIN1 Proteins)-G620R-containing NMDARs after birth.
These preliminary results demonstrated that the GRIN2B gene may confer to some extent the susceptibility to OCD and its symptoms.
Our finding confirms that early-onset EE may be caused not only by gain-of-function variants but also by splice site mutations-in particular those affecting the splice acceptor site of the 10th intron of the GRIN2B gene.
Results indicate that the GRIN2B single nucleotide polymorphisms rs890 might be associated with schizophrenia in the Chinese Han population.
These in vivo changes reflect changes in glutamate transporter (show SLC1A1 Proteins) protein (show HNRNPU Proteins) in Huntington's disease (HD), mice and human HD post-mortem tissue. Furthermore, NAC was able to rescue (show GRIN1 Proteins)changes in key glutamate receptor proteins related to excitotoxicity in HD, including NMDAR2B.
Genetic association of CYP2B6 (show CYP2B6 Proteins)*6 and GRIN2B (rs1019385 and rs1806191) single-nucleotide polymorphisms and ketamine-induced EP occurrence.
most rare variants in GluN2A (show GRIN2A Proteins) were associated with epilepsy, whereas GluN2B variants were associated with intellectual disability with or without seizures
In this review, mutations in GRIN2B were described as distributed throughout the entire gene in patients with neuropsychiatric and developmental disorders.
Negative regulation of REST on NR2B in spinal cord takes part in the exacerbation of bone cancer pain.
results demonstrated that phosphorylation level of S1284 in GluN2B was regulated by acute stress
study are the first to demonstrate that phosphorylation of GluN2B subunit at Tyr1472 is important for trigeminal transmission of itch and suggest that the NMDA receptor activation occurs upstream of the receptor of gastrin-releasing peptide (GRP)-GRP (show GRP Proteins) receptor pathway
GluN2B gene deletion mice consumed significantly less alcohol, than non-mutant controls.
Neonatal hypoxic-ischemia reshaped the postsynaptic GluN2B interactome by recruiting new proteins, including multiple kinases, into the complexes
Sepsis selectively decreased the protein and mRNA levels of GluN2A (show GRIN2A Proteins), GluN2B and GluN1 (show GRIN1 Proteins) but not the levels of synaptophysin (show SYP Proteins) or the neuronal number in the hippocampus of septic mice.
Drebrin A (show DBN1 Proteins) can be found co-clustering with NR2B-containing NMDARs at the plasma membrane, while NR2A (show GRIN2A Proteins)-containing NMDARs co-traffic into the spine cytoplasm but do not co-cluster at the plasma membrane.
Overexpression of EphB2 (show EPHB2 Proteins) also rescued the ADDLs-induced depletion of the expression of EphB2 (show EPHB2 Proteins) and GluN2B-containing NMDA receptors trafficking in cultured hippocampal neurons.
PGRN (show GRN Proteins) decrease, resulting from pathogenic mutations, might compromise the trophism of cortical neurons by affecting GluN2B-contaning NMDA receptors
HumanTau(AT) causes excitotoxicity mediated by NR2B-containing NMDA receptors due to enhanced extracellular glutamate (show GRIN1 Proteins).
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.
NMDA type glutamate receptor
, N-methyl D-aspartate receptor subtype 2B
, N-methyl-D-aspartate receptor subunit 2B
, glutamate [NMDA] receptor subunit epsilon-2
, glutamate receptor ionotropic, NMDA 2B
, N-methyl-D-aspartate receptor subunit 3
, glutamate receptor subunit epsilon-2
, glutamate receptor, ionotropic, NMDA2B
, N-methyl-D-aspartate receptor subunit NR2B
, N-methyl D-aspartate receptor 2B