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GRIN2B

Official Full Name
glutamate ionotropic receptor NMDA type subunit 2B
Organism
Homo sapiens
GeneID
2904
Background
This gene encodes a member of the N-methyl-D-aspartate (NMDA) receptor family within the ionotropic glutamate receptor superfamily. The encoded protein is a subunit of the NMDA receptor ion channel which acts as an agonist binding site for glutamate. The NMDA receptors mediate a slow calcium-permeable component of excitatory synaptic transmission in the central nervous system. The NMDA receptors are heterotetramers of seven genetically encoded, differentially expressed subunits including NR1 (GRIN1), NR2 (GRIN2A, GRIN2B, GRIN2C, or GRIN2D) and NR3 (GRIN3A or GRIN3B). The early expression of this gene in development suggests a role in brain development, circuit formation, synaptic plasticity, and cellular migration and differentiation. Naturally occurring mutations within this gene are associated with neurodevelopmental disorders including autism spectrum disorder, attention deficit hyperactivity disorder, epilepsy, and schizophrenia. [provided by RefSeq, Aug 2017]
Synonyms
NR3; MRD6; NR2B; hNR3; DEE27; EIEE27; GluN2B; NMDAR2B;
Bio Chemical Class
Glutamate-gated ion channel
Protein Sequence
MKPRAECCSPKFWLVLAVLAVSGSRARSQKSPPSIGIAVILVGTSDEVAIKDAHEKDDFHHLSVVPRVELVAMNETDPKSIITRICDLMSDRKIQGVVFADDTDQEAIAQILDFISAQTLTPILGIHGGSSMIMADKDESSMFFQFGPSIEQQASVMLNIMEEYDWYIFSIVTTYFPGYQDFVNKIRSTIENSFVGWELEEVLLLDMSLDDGDSKIQNQLKKLQSPIILLYCTKEEATYIFEVANSVGLTGYGYTWIVPSLVAGDTDTVPAEFPTGLISVSYDEWDYGLPARVRDGIAIITTAASDMLSEHSFIPEPKSSCYNTHEKRIYQSNMLNRYLINVTFEGRNLSFSEDGYQMHPKLVIILLNKERKWERVGKWKDKSLQMKYYVWPRMCPETEEQEDDHLSIVTLEEAPFVIVESVDPLSGTCMRNTVPCQKRIVTENKTDEEPGYIKKCCKGFCIDILKKISKSVKFTYDLYLVTNGKHGKKINGTWNGMIGEVVMKRAYMAVGSLTINEERSEVVDFSVPFIETGISVMVSRSNGTVSPSAFLEPFSADVWVMMFVMLLIVSAVAVFVFEYFSPVGYNRCLADGREPGGPSFTIGKAIWLLWGLVFNNSVPVQNPKGTTSKIMVSVWAFFAVIFLASYTANLAAFMIQEEYVDQVSGLSDKKFQRPNDFSPPFRFGTVPNGSTERNIRNNYAEMHAYMGKFNQRGVDDALLSLKTGKLDAFIYDAAVLNYMAGRDEGCKLVTIGSGKVFASTGYGIAIQKDSGWKRQVDLAILQLFGDGEMEELEALWLTGICHNEKNEVMSSQLDIDNMAGVFYMLGAAMALSLITFICEHLFYWQFRHCFMGVCSGKPGMVFSISRGIYSCIHGVAIEERQSVMNSPTATMNNTHSNILRLLRTAKNMANLSGVNGSPQSALDFIRRESSVYDISEHRRSFTHSDCKSYNNPPCEENLFSDYISEVERTFGNLQLKDSNVYQDHYHHHHRPHSIGSASSIDGLYDCDNPPFTTQSRSISKKPLDIGLPSSKHSQLSDLYGKFSFKSDRYSGHDDLIRSDVSDISTHTVTYGNIEGNAAKRRKQQYKDSLKKRPASAKSRREFDEIELAYRRRPPRSPDHKRYFRDKEGLRDFYLDQFRTKENSPHWEHVDLTDIYKERSDDFKRDSVSGGGPCTNRSHIKHGTGDKHGVVSGVPAPWEKNLTNVEWEDRSGGNFCRSCPSKLHNYSTTVTGQNSGRQACIRCEACKKAGNLYDISEDNSLQELDQPAAPVAVTSNASTTKYPQSPTNSKAQKKNRNKLRRQHSYDTFVDLQKEEAALAPRSVSLKDKGRFMDGSPYAHMFEMSAGESTFANNKSSVPTAGHHHHNNPGGGYMLSKSLYPDRVTQNPFIPTFGDDQCLLHGSKSYFFRQPTVAGASKARPDFRALVTNKPVVSALHGAVPARFQKDICIGNQSNPCVPNNKNPRAFNGSSNGHVYEKLSSIESDV
Open
Disease
Alpha-1-antitrypsin deficiency, Alzheimer disease, Cardiac arrest, Cerebral ischaemia, Cerebral ischaemic stroke, Chronic pain, Depression, Dissociative neurological symptom disorder, Epilepsy/seizure, General pain disorder, Intracranial injury, Multiple sclerosis, Neurodegenerative disorder, Neuropathy, Parkinsonism
Approved Drug
1 +
Clinical Trial Drug
8 +
Discontinued Drug
14 +

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Detailed Information

Located on chromosome 12, the GRIN2B gene encodes the NMDA receptor's NR2B component. Part of the ionotropic glutamate receptor family, NMDA receptors operate as ligand-gated ion channels. Mainly by means of calcium ions, which are vital for controlling many brain functions including synaptic plasticity, these receptors are absolutely vital for mediating excitatory synaptic transmission.

NMDA Receptor Composition and Function

NMDA receptors are heterotetramers, meaning they are composed of four subunits, usually a combination of NR1, NR2, and/or NR3. The NR2B subunit is particularly crucial because it determines the receptor's kinetic properties and ion permeability. It also affects receptor spread along the neuronal membrane. High amounts of NR2B during brain development help activities like neuronal migration, synapse creation, and differentiation, hence stressing its function in the architecture of the growing brain.

GRIN2B's participation in early embryonic development implies that it helps to establish the basic brain circuits supporting more advanced activities like cognition and sensory processing. Its significant presence in the hippocampus and prefrontal cortex—brain areas linked to learning and memory—underscores its relevance even beyond the embryonic period into maturity.

Figure 1 illustrates the molecular mechanisms of the early and later phases of long-term potentiation (LTP).Figure 1. A model illustrating the molecular mechanisms of the early and later phases of long-term potentiation (LTP). (Huang M, et al., 2022)

GRIN2B and Neurodevelopmental Disorders

Mutations within the GRIN2B gene are linked to various neurodevelopmental disorders. These disorders arise due to their critical role in managing synaptic functions and neural communication pathways. Understanding these associations offers insights into potential treatment strategies.

Autism Spectrum Disorder (ASD)

Comprising many complicated developmental disorders, ASD is characterized by difficulties in social interaction, communication, and repetitive activities. By influencing synaptic plasticity and neuronal connection, GRIN2B mutations help ASD by perhaps causing the unusual neural circuit found in autism. Research helps to guide the creation of focused treatments by means of the identification and comprehension of these mutations.

Intellectual Disability (ID)

Intellectual impairment is defined by notable deficits in both intellectual capacity and adaptive conduct. GRIN2B mutations could lower NMDA receptor function, which would impair information processing and brain growth required for cognition. Understanding gene-related pathways and early intervention may assist to control and reduce ID consequences.

Epilepsy

Another disease connected to GRIN2B mutations is epilepsy, defined by persistent seizures. These mutations' altered NMDA receptor function may cause too much neuronal firing, hence causing seizure attacks. Treatments that change receptor function could help epilepsy sufferers with certain hereditary disorders.

Schizophrenia and ADHD

Emerging studies show potential links between GRIN2B variations and other psychiatric disorders, such as schizophrenia and attention deficit hyperactivity disorder (ADHD). These conditions may also be influenced by disrupted neural pathways regulated by NMDA receptor activity, making GRIN2B a target for research.

Therapeutic Approaches and Future Directions

Understanding GRIN2B's role in neural processes opens up avenues for therapeutic interventions. Targeted therapeutics for conditions linked with GRIN2B mutations might be developed via advances in gene therapy, pharmacology, and neuroimaging.

Tools for fixing bad mutations within the GRIN2B gene might be found in genome editing technologies such as CRISPR-Cas9. Moreover, medicines that change NMDA receptor activity might cure associated conditions by regulating receptor function and lowering symptoms.

New knowledge on how GRIN2B mutations change brain structure and function is provided by neuroimaging advances, hence supporting early diagnosis and therapy creation. With the possibility to greatly improve our knowledge of cognitive and neurological health, ongoing study into GRIN2B keeps untangling the complexity of its impact on the brain.

Understanding brain development and function depends much on the GRIN2B gene. Its influence on neurodevelopmental diseases and cognitive functions is underlined by its involvement in NMDA receptor activation. Promising treatment ideas are on the horizon for tackling the genetic basis of many diseases with ongoing research and technical developments.

References:

  1. Lemke JR, Geider K, Helbig KL, et al. Delineating the GRIN1 phenotypic spectrum: A distinct genetic NMDA receptor encephalopathy. Neurology. 2016 Jun 7;86(23):2171-8.
  2. Huang M, Li Z, Zhu H. Recent Advances of Graphene and Related Materials in Artificial Intelligence. Adv Intell Syst. 2022 Jun 26.
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