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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.
Genetic variants were found in GluN2B from patients with neurological or psychiatric disorders resulting in reduced surface expression of GluN2B.
Results found that GluN2B subunit-containing NMDARs were dominant in induced pluripotent stem cell-derived neurons and that tyrosine-protein kinase Fyn (show FYN Proteins) potentiated the function of GluN2B subunit-containing NMDARs.
Multiple genetic variants in GRIN2B are jointly associated with gene expression, prefrontal function and behaviour during working memory (WM). These results support the role of GRIN2B genetic variants in WM prefrontal activity in human adults.
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).
The NR2B-CREB (show CREB1 Proteins)-miR212/132-CRTC1 (show CRTC1 Proteins)-CREB (show CREB1 Proteins) signal network plays an important role in the regulation of pain.
This study demonstrated that Increasing the GluN2A (show GRIN2A Proteins)/GluN2B Ratio in Neurons of the Mouse Basal and Lateral Amygdala Inhibits the Modification of an Existing Fear Memory Trace.
These in vivo changes reflect changes in glutamate transporter (show SLC1A1 Proteins) protein (show LAPTM4A Proteins) in HD mice and human HD post-mortem tissue. Furthermore, NAC was able to rescue changes in key glutamate (show GRIN1 Proteins) receptor proteins related to excitotoxicity in HD, including NMDAR2B.
Data show that hydroxyproline HyP (show PHEX Proteins)(10) plays a critical role in maintaining the structural integrity of conantokins conRl-B, which can be correlated with its glutamate (show GRIN1 Proteins) receptor, ionotropic, N-methyl D-aspartate 2B (GluN2B) subunit-selective inhibition.
These results highlight the requirement for stringent pharmacogenetic approaches to separate specific on-target effects from nonspecific off-target effects. Importantly, they also demonstrate that the CaMKII (show CAMK2G Proteins)/GluN2B interaction is required not only for normal long-term potentiation induction but also for the maintenance of synaptic strength.
GluN2B-dependent calcium signaling and excitatory postsynaptic current, long-term depression, and spatial reversal learning are enhanced in the hippocampus of AC6 (show ADCY6 Proteins)(-/-) mice without altering the gross anatomy of the brain
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