GRID2 Antibodies

Structure of GRID2

The glutamate receptor δ2 subunit (GluD2) encoded by the GRID2 gene is a transmembrane protein with a molecular weight of approximately 130 kDa. Its precise molecular weight may vary slightly among different species or splicing variants.

The GRID2 protein is composed of approximately 1000 amino acids. This protein forms transsynaptic connections through the extracellular Cbln1-neurexin complex. Its unique atypical ion channel mechanism distinguishes it from other glutamate receptors and is crucial for maintaining the synaptic function of cerebellar Purkinfield cells.

Fig. 1 Structural Analysis of GRID2 Receptor Monomer Reveals Key Extracellular Domain Deletion.¹

Key structural properties of GRID2:

• N-terminal domain
• Ligand binding domain
• Transmembrane zone
• C-end PDZ binding domain

Functions of GRID2

The main function of the GRID2 gene is to regulate cerebellar synaptic plasticity and motor coordination, but it is also involved in a variety of key physiological and pathological processes in the nervous system.

Unlike typical ionic glutamate receptors, GRID2 does not rely on glutamate activation but triggers downstream signals through cross-synaptic adhesion molecule interactions. Its unique "non-channel" function provides a new molecular mechanism perspective for synaptic regulation.

Applications of GRID2 and GRID2 Antibody in Literature

1. Koh, Kishin, et al. "A heterozygous GRID2 mutation in autosomal dominant cerebellar ataxia." Human Genome Variation 9.1 (2022): 27. https://doi.org/10.1038/s41439-022-00204-x

The article indicates that heterozygous mutations in the GRID2 gene can lead to autosomal dominant cerebellar ataxia (ADCA). The first Algerian family presented with ataxia accompanied by cognitive impairment and hearing loss, while the newly discovered Japanese family only showed simple cerebellar ataxia, suggesting that GRID2 mutation screening should be extended to simple ADCA cases.

2. Allen, James P., et al. "Clinical features, functional consequences, and rescue pharmacology of missense GRID1 and GRID2 human variants." Human molecular genetics 33.4 (2024): 355-373.https://doi.org/10.1093/hmg/ddad188

The article indicates that the GRID2 gene encodes the GluD2 receptor, and its variation can lead to abnormal neurodevelopment. Research has found that mutations in the GRID2 M3 domain (such as A654T) can trigger persistent receptor activation, similar to the lurcher mutation phenotype. The compound pentamidine can effectively suppress the abnormal current (IC50 at 50 nM) of GluD2-T649A, providing new ideas for the treatment of related diseases.

3. Ali, Zafar, et al. "Homozygous GRID2 missense mutation predicts a shift in the D-serine binding domain of GluD2 in a case with generalized brain atrophy and unusual clinical features." BMC Medical Genetics 18.1 (2017): 144.https://doi.org/10.1186/s12881-017-0504-6

Researchers have found that the novel homozygous missense mutation of GRID2 [c.2128C>T, p.(Arg710Trp)] leads to autosomal recessive cerebellar ataxia. The patient presented with slow-progressive ataxia that began in childhood and was accompanied by psychomotor developmental delay. MRI showed extensive brain atrophy, expanding the phenotypic spectrum of GRID2-related cerebellar syndrome.

4. Kumagai, Ayako, et al. "Altered actions of memantine and NMDA-induced currents in a new Grid2-deleted mouse line." Genes 5.4 (2014): 1095-1114. https://doi.org/10.3390/genes5041095

Research has found that mice with GRID2 gene deletion mutations exhibit ataxia and balance disorders, and memantine (10mg/kg) exacerbates their symptoms. Electrophysiological experiments have shown that the absence of GRID2 leads to abnormal function of NMDA receptors in granulosa cells, while the activation of AMPA receptors enhances the sensitivity of wild-type mice to megamine, suggesting the key role of GRID2 in regulating the function of glutamate receptors.

5. Grigorenko, Anastasia P., et al. "Neurodevelopmental syndrome with intellectual disability, speech impairment, and Quadrupedia is associated with glutamate Receptor Delta 2 gene defect." Cells 11.3 (2022): 400.https://doi.org/10.3390/cells11030400

Researchers have found that a 36.2kb homozygous deletion of the GRID2 gene leads to a unique "atavistic" phenotype, characterized by quadrupedal walking, intellectual disability and language loss. This deficiency causes defects in the amino-terminal domain of the GRID2 protein, affecting protein folding and transport. Evolutionary analysis shows that the GRID2 gene may have acquired specific mutations during human evolution to enhance mRNA stability.

Creative Biolabs: GRID2 Antibodies for Research

Creative Biolabs specializes in the production of high-quality GRID2 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom GRID2 Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our GRID2 antibodies, custom preparations, or technical support, contact us at email.