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- Table of Contents
Facts about Glutamate receptor 3.
Binding of the excitatory neurotransmitter L- glutamate induces a conformation change, resulting in the opening of the cation channel, and thereby transforms the chemical signal to an electrical impulse. The receptor then desensitizes quickly and enters a transient inactive state, characterized by the presence of bound agonist.
Human | |
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Gene Name: | GRIA3 |
Uniprot: | P42263 |
Entrez: | 2892 |
Belongs to: |
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glutamate-gated ion channel (TC 1.A.10.1) family |
AMPA 3; AMPA3; AMPA-selective glutamate receptor 3; GluA3; GluR3; GluR-3; GLURC; GLUR-C; GLUR-K3; glutamate receptor C; glutamate receptor subunit 3; glutamate receptor, ionotrophic, AMPA 3; GRIA3
Mass (kDA):
101.157 kDA
Human | |
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Location: | Xq25 |
Sequence: | X; NC_000023.11 (123184243..123490915) |
Cell membrane; Multi-pass membrane protein. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein. Interaction with CNIH2 and CNIH3 promotes cell surface expression.
The Anti-Glutamate receptor 3 (GRIA3) marker is an excellent way to determine whether or not a substance is addictive. Boster Bio offers several advantages over other products in this regard. Scientists can submit results for special samples and species and applications and receive product credits. In addition, this marker is available for scientists worldwide. Read on to learn more about this groundbreaking technology. After all, addiction is a serious issue for so many people.
The Anti-Glutamate receptor 3/ GRIA3 marker in Boster Bio was validated with the mouse model. The antibody has been tested for WB applications. It has cross-reactivity with Human, Mouse, and Rat. It is highly suitable for use in research, immunohistochemistry, and protein analysis. The boster bio antibody is available in both diluted forms for WB applications.
Various studies have implicated the role of the anti-Glutamate receptor antibody in the development of autoimmune and neurological diseases. This molecule is critical for many neuronal functions and when produced in excess quantities, causes massive damage to the brain. Several CNS disorders are characterized by anti-GRIA3 antibodies. The antibodies are known to impair neuronal signaling, induce brain damage, and contribute to various neurological disorders.
The expression of glutamate receptor genes has a complex pattern of expression in human brains. This highly regulated gene expression requires maintenance over many decades. One mechanism for the maintenance of highly regulated gene expression is differential methylation of lysine residues on the N-terminal tails of histone proteins. To unravel the role of this epigenetic mark in long-term gene regulation, we used native chromatin immunoprecipitation assay. We used human cerebellar cortex samples ranging in age from midgestation to 90 years old.
To study the alternative exons of GRIA3, we used bisulfite genomic sequencing. We designed primers for GRIA3 using Methyl Primer Express v.1.0 software from Thermo Research and Thermo Fisher Scientific. Next, we used the EZ DNA Methylation-Gold Kit to induce the chemical conversion of cytosine to uracil. We then amplified 200-300-bp pairs of GRIA3 with Immolase DNA polymerase in a final volume of 15 mL for 40 cycles.
This gene is responsible for the production of glutamate by human cells. It is involved in learning and memory. Mutations in glutamate receptors have been associated with brain disorders such as Alzheimer's disease. The gene encoding GRIA3 is related to a well-known AD SNP. Therefore, identifying GRIA3 in human blood may provide a more complete understanding of the disease and possible treatments.
The first human clinical trials using the GRIA3 marker identified a patient with a balanced translocation, bipolar disorder, and X-linked mental retardation. The patient was a 20-year-old Iranian woman, and she had developed a bipolar affective disorder by the time she was 12 years old. The patient showed symptoms of cyclic vomiting, and the translocation involved the Xq24 region.
Genetic studies of genes have shown that genetic variants influencing sleep are important for better understanding of physiological processes that govern sleep and wake cycles. In one case, a large clinical sequencing project was used to sequence the genes of children with an extremely delayed sleep-wake cycle and very long wake and sleep periods. This family was found to have a novel missense mutation in the GRIA3 gene, which is responsible for intellectual disability.
Several studies also revealed that polymorphisms in glutamatergic genes were associated with decreased libido, difficulty achieving an erection, and difficulty achieving an orgasm. This result triggered widespread reassessment of antidepressant prescription practices. Despite this concern, only two individuals who enrolled in the STAR*D study attempted suicide. Of these, one of them, who had been recruited through DNA collection, denied any suicidal ideation. However, she did carry high-risk alleles in the GRIA3 gene.
The GRIA3 gene has eight coding SNPs in different LD-blocks, primarily located within the promoter region and intron 2. Two G/A SNPs, rs12559450 and rs4825840, are located in the promoter region of the gene. Both mutations are located within the intron 2 region of the gene. Price of the GRIA3 marker varies by vendor and is discussed below.
PMID: 7918660 by Rampersad V., et al. Human glutamate receptor hGluR3 flip and flop isoforms: cloning and sequencing of the cDNAs and primary structure of the proteins.
PMID: 10644433 by Gecz J., et al. Characterization of the human glutamate receptor subunit 3 gene (GRIA3), a candidate for bipolar disorder and nonspecific X-linked mental retardation.