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Mouse Anti-GRIA2 (AA 652-807) Recombinant Antibody (CBFYH-3477) (CBMAB-H4025-FY)

This product is mouse antibody that recognizes GRIA2. The antibody CBFYH-3477 can be used for immunoassay techniques such as: ELISA, FC, WB.
See all GRIA2 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-3477
Antibody Isotype
IgG1
Application
ELISA, FC, WB

Basic Information

Immunogen
Purified recombinant fragment of human GRIA2 (AA: 652-807) expressed in E. coli
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS
Preservative
0.05% Sodium azide
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 652-807

Target

Full Name
Glutamate ionotropic receptor AMPA type subunit 2
Introduction
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, GRIA1-4. The subunit encoded by this gene (GRIA2) is subject to RNA editing (CAG->CGG; Q->R) within the second transmembrane domain, which is thought to render the channel impermeable to Ca(2+).
Entrez Gene ID
2891
UniProt ID
P42262
Alternative Names
GLUR2; GLURB; GluA2; HBGR2; GluR-K2
Function
Receptor for glutamate that functions as ligand-gated ion channel in the central nervous system (PubMed:31300657).

It plays an important role in excitatory synaptic transmission. L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. Binding of the excitatory neurotransmitter L-glutamate induces a conformation change, leading to the opening of the cation channel, and thereby converts the chemical signal to an electrical impulse. The receptor then desensitizes rapidly and enters a transient inactive state, characterized by the presence of bound agonist. In the presence of CACNG4 or CACNG7 or CACNG8, shows resensitization which is characterized by a delayed accumulation of current flux upon continued application of glutamate. Through complex formation with NSG1, GRIP1 and STX12 controls the intracellular fate of AMPAR and the endosomal sorting of the GRIA2 subunit toward recycling and membrane targeting (By similarity).
Biological Process
Chemical synaptic transmission Source: ProtInc
Ionotropic glutamate receptor signaling pathway Source: UniProtKB
Signal transduction Source: ProtInc
Synaptic transmission, glutamatergic Source: ARUK-UCL
Cellular Location
Cell membrane; Postsynaptic cell membrane; Postsynaptic density membrane; Endoplasmic reticulum membrane. Interaction with CACNG2, CNIH2 and CNIH3 promotes cell surface expression (By similarity). Displays a somatodendritic localization and is excluded from axons in neurons (By similarity).
Involvement in disease
Neurodevelopmental disorder with language impairment and behavioral abnormalities (NEDLIB):
A neurodevelopmental disorder characterized by global developmental delay, impaired intellectual development, poor or absent speech, and behavioral abnormalities, such as autism spectrum disorder, repetitive behaviors, and hyperactivity. Some patients develop seizures and manifest developmental regression.
Topology
Extracellular: 25-543
Helical: 544-564
Cytoplasmic: 565-591
Helical: 592-607
Extracellular: 608-610
Helical: 611-616
Cytoplasmic: 617-637
Helical: 638-812
Extracellular: 813-833
Helical: 834-883
PTM
Palmitoylated. Depalmitoylated upon glutamate stimulation. Cys-610 palmitoylation leads to Golgi retention and decreased cell surface expression. In contrast, Cys-836 palmitoylation does not affect cell surface expression but regulates stimulation-dependent endocytosis (By similarity).
Phosphorylation at Tyr-876 is required forc interaction with IQSEC1 and ARF6 activation.

Fang, X., Yang, S., Chen, M., Sun, R., Zhao, L., Gu, B., ... & Zhao, Y. (2023). Association analysis of polymorphisms at GLRB, GRIA2, and GASK1B genes with reproductive traits in Dazu Black Goats. Animal Biotechnology, 1-9.

Coombs, I. D., Ziobro, J., Krotov, V., Surtees, T. L., Cull‐Candy, S. G., & Farrant, M. (2022). A gain‐of‐function GRIA2 variant associated with neurodevelopmental delay and seizures: Functional characterization and targeted treatment. Epilepsia.

Latsko, M. S., Koboldt, D. C., Franklin, S. J., Hickey, S. E., Williamson, R. K., Garner, S., ... & Wilson, R. K. (2022). De novo missense variant in GRIA2 in a patient with global developmental delay, autism spectrum disorder, and epileptic encephalopathy. Molecular Case Studies, 8(4), a006172.

Cai, Q., Zhou, Z., Luo, R., Yu, T., Li, D., Yang, F., & Yang, Z. (2022). Novel GRIA2 variant in a patient with atypical autism spectrum disorder and psychiatric symptoms: a case report. BMC pediatrics, 22(1), 1-8.

Li, X., Chen, W., Yu, Q., Zhang, Q., Zhang, T., Huang, X., ... & Lu, Y. (2021). A circuit of mossy cells controls the efficacy of memory retrieval by Gria2I inhibition of Gria2. Cell Reports, 34(7), 108741.

Alkelai, A., Shohat, S., Greenbaum, L., Schechter, T., Draiman, B., Chitrit-Raveh, E., ... & Kohn, Y. (2021). Expansion of the GRIA2 phenotypic representation: a novel de novo loss of function mutation in a case with childhood onset schizophrenia. Journal of Human Genetics, 66(3), 339-343.

Zhou, M., Qi, L., & Gu, Y. (2021). GRIA2/ENPP3 Regulates the Proliferation and Migration of Vascular Smooth Muscle Cells in the Restenosis Process Post-PTA in Lower Extremity Arteries. Frontiers in Physiology, 12, 712400.

Tischbein, M., Baron, D. M., Lin, Y. C., Gall, K. V., Landers, J. E., Fallini, C., & Bosco, D. A. (2019). The RNA-binding protein FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for GRIA2 mRNA processing. Journal of Biological Chemistry, 294(26), 10194-10210.

Zhang, Y., Wang, K., Zhao, Z., Sun, S., Zhang, K., Huang, R., ... & Hu, H. (2018). ADAR3 expression is an independent prognostic factor in lower-grade diffuse gliomas and positively correlated with the editing level of GRIA2 Q607R. Cancer Cell International, 18, 1-12.

Capauto, D., Colantoni, A., Lu, L., Santini, T., Peruzzi, G., Biscarini, S., ... & Bozzoni, I. (2018). A regulatory circuitry between Gria2, miR-409, and miR-495 is affected by ALS FUS mutation in ESC-derived motor neurons. Molecular neurobiology, 55, 7635-7651.

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For research use only. Not intended for any clinical use.

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