GRIN2A Antibodies

Glutamate receptor ionotropic, NMDA 2A (GRIN2A)

Part of NMDA receptor complexes that serve as heterotetrameric, ligand-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Channel activation requires binding of the neurotransmitter glutamate to the epsilon subunit, glycine binding to the zeta subunit, plus membrane depolarization to get rid of channel inhibition by Mg(2+) (PubMed:8768735, PubMed:26919761, PubMed:26875626, PubMed:28105280).

Sensitivity to glutamate and channel kinetics are determined by the subunit composition; stations comprising GRIN1 and GRIN2A have higher sensitivity to glutamate and faster kinetics than channels formed by GRIN1 and GRIN2B (PubMed:26919761, PubMed:26875626). Contributes to the slow stage of excitatory postsynaptic current, long-term synaptic potentiation, and learning (By similarity).

Gene Information

Human
Gene Name:	GRIN2A
Uniprot:	Q12879
Entrez:	2903

Family

Belongs to:
glutamate-gated ion channel (TC 1.A.10.1) family

Alternative Names

glutamate receptor, ionotropic, N-methyl D-aspartate 2A; hNR2A; NMDA receptor subtype 2A; N-methyl D-aspartate receptor subtype 2A; N-methyl-D-aspartate receptor subunit 2A; subunit epsilon-1

Molecular Weight

Mass (kDA):
165.283 kDA

Genomic Context

Human
Location:	16p13.2
Sequence:	16; NC_000016.10 (9753404..10182928, complement)

Subcellular Localizations

Cell projection, dendritic spine. Cell membrane; Multi-pass membrane protein. Cell junction, synapse. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein. Cytoplasmic vesicle membrane. Expression at the dendrite cell membrane and at synapses is regulated by SORCS2 and the retromer complex.

Diseases

• Schizophrenia
• Bipolar Disorder
• Mental Disorders
• Attention Deficit Hyperactivity Disorder
• Autistic Disorder
• Huntington Disease
• Epilepsy
• Endoplasmic Reticulum Stress
• Malignant Neoplasms
• Neoplasms
• Dysequilibrium Syndrome
• Pcp - Hallucinogen-related Disorder

• Tissue Adhesions
• Lingual-facial-buccal Dyskinesia
• Autism Spectrum Disorders
• Malnutrition
• Dyskinetic Syndrome
• Epilepsy, Rolandic
• Landau-kleffner Syndrome

Interacting Proteins

• Dlg3
• DLG4
• Dlg4
• LRP1

Pathways

• Brain Development
• Pathogenesis
• Localization
• Short-term Memory
• Translation
• Cell Adhesion
• Cell Proliferation
• Catecholamine Secretion
• Aging
• Glycosylation
• Synaptic Transmission
• Inflammatory Response

• Protein Glycosylation
• Swimming
• Regulation Of Histone Acetylation
• Histone Acetylation
• Regulation Of Synaptic Activity
• Cognition
• Secretion

PTMs

• Phosphorylation
• Reduction

• Glycosylation
• Acetylation

Research Areas

• Neuroendocrinology
• Neuronal Cell Markers
• Neuroscience
• Neurotransmission
• Vision

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/GRIN2A

Boster Bio: Best Uses Of The Grind2A Marker

In this article, we'll talk about the Boster Bio: Best Uses of the Grind2A Marker its methods, applications, and the costs. This article will help you understand how to utilize this marker. We will also talk about how this marker can be used to measure the capacity of a protein's undergo redox.

Boster Bio: GRIN2A marker

GluN2A is a protein that affects signaling in regions of the brain that control speech. It can also affect brain activity during sleep, which can trigger various symptoms. GluN2A is involved in speech, and the changes in this protein can cause mild or severe impairments. This article will review how to make the most of the GRIN2A marker in the laboratory.

Methods

The GRIN2A gene codes for the GluN2A protein, which is a component of the NMDA receptor. This protein is found in the brain and spinal cord and is an integral part of a subset of NMDA receptors. The flow of glutamate cations stimulates neurons. A single gene that encodes GRIN2A was the focus of this study.

HEK cells were transiently infected with a variety of GRIN2A mutant constructs and the co-transfection with empty vector (EV) and GRIN1 resulted in cell death after 48 hours. Live-cell imaging was carried out using the IncuCyte imaging system and images were taken at a 20-fold magnification. The images presented are representative time events of cell death normalized to the confluency of the HEK cells in each well.

A number of SNPs within the GRIN2A gene have been associated with drug addiction. SNPs that alter transcription factors binding can cause motifs to be altered and may be related to dependence on substances. However, the GRIN2A marker is not yet widely used to aid in this process. To perform this task researchers must first locate an entire population that has a large number of people affected and then analyze their genotypes and allele frequencies to find out which SNPs are associated with the possibility of developing a drug-dependence.

The GRIN2A gene has been linked to a range of neurologic disorders including LKS, BECTS, and CSWSS. GRIN2A missense mutations have been associated with epilepsy. These findings could provide further insights into gene-phenotype correlations. The electrophysiological analysis and therapeutic potential of GRIN2A mutations can be useful.

Researchers recently conducted a study that compared four previously undiscovered single nucleotide variation variants in the subunit gene NMDA-R. Two of these variants had never previously been examined. Researchers were interested in knowing whether these variants were related to cognitive impairment in schizophrenia. The results of the study, although preliminary, suggest that GRIN1 could be a promising candidate gene for schizophrenia.

Applications

The GRIN2A gene, a new marker, offers new insights into the causes of GRIN2A gain-of-function disorder. The new marker was identified using genetic modeling, a method that provides complementary methods for testing novel therapies. The findings of this study demonstrate that the GRIN2A gene is vital for neurodevelopmental disorderssuch as the autism spectrum and fetal loss.

EAS mutations may have distinct functional effects. Missense mutations can lead to more severe disorders, and Truncation mutations can cause more severe conditions. There are many other factors that can affect severity of the phenotypes. One study found memantine, an NMDA receptor antagonist, decreased seizures and also improved other symptoms in patients suffering from GRIN2A encephalopathy. However, further research is necessary to determine whether memantine may have an effect on other diseases or phenotypes.

Researchers have discovered a GRIN2A–L812M mutation in a gene encoding GluN2A. This mutation was found in a patient suffering from severe epilepsy. The mutation increased the agonist's potency however it decreased the susceptibility to zinc or magnesium. Homozygous mutant mice also developed epileptic encephalopathy and had lethal tonic-clonic seizures after three weeks.

Mutations in the GRIN2A gene alter the response to glutamate and glycine. Single-cell calcium flux imaging (CFI) shows different responses to glutamate and glycine. The graph shows the individual cell traces in red and cyan. In addition, a normalized concentration response curve shows decreased potential for agonists and no glutamate binding activity.

Live-cell imaging of HEK cells transfected with the GRIN2A plasmid has shown similar results when the receptors were co-transfected with the pcDNA3.1 (+) vector. The mutations were not seen in HEK cells transfected using the empty vector. A calcium flux assay was performed to assess the efficacy of the transfections. HEK-293 cells were exposed for a short period of time to MgATP and maximally glutamate to determine their efficacy. The number of HEK cells that responded to MgATP was also utilized to determine the efficiency of transfection.

Mutations in GRIN2A are associated with seizures and epilepsies idiopathic focal as well as neurodevelopmental disorders. These diseases are characterized by GRIN2A according to three research groups. Although the GRIN2A gene could be an uncommon one but a phenotypic range of these diseases has been identified. The gene gives instructions for the production of GluN2A protein, which is one subunit of the NMDA receptor. The GluN2A protein determines the position and function of NMDA receptors.

Cost

The GRIN2A gene is an alternative DNA variant that affects the brain's NMDA receptor. Patients with mutations in this gene have an increased risk of developing epilepsy, or developmental differences. This variant causes abnormalities in NMDA receptor function, and therefore it is important to identify patients affected. However, the cost associated with this gene variant could restrict its use for research purposes.

GRIN2D is expressed in the vessels of around 40 percent of colorectal cancers. It is only found in ten percent of healthy colon samples. This suggests that GRIN2D could be targeted at the cancer's vessels but the gene is expressed in many healthy tissues. It is vital to watch it carefully to ensure that it doesn't cause harm to normal tissues. This marker has a myriad of potential applications in the field of treatment for cancer.

GRIN2A has been associated with mental illnesses and cancers. It is linked to cognitive impairment in people who suffer from schizophrenia. However, the cost of this marker is still quite high. It is currently the most costly genetic marker in the history of mankind as of the time of writing. The price of the GRIN2A marker is based on the amount of research that is conducted on it. However, the results are promising and can be used in clinical trials to test patients.

The GRIN2A gene has ten SNPs. One of these variants, rs1375067, demonstrated a significant difference between heroin dependence and controls. Despite the fact that both genotypes had significant differences, it was difficult to determine the variant that caused them. Regulome DB as well as HaploReg Software both suggested that the SNPs alter the motifs that encode GRIN2A genes, possibly affecting transcription factors.