Rabbit Anti-GRIA2 Recombinant Antibody (CBNH-057) (CBMAB-R4382-CN)

Name: Rabbit Anti-GRIA2 Recombinant Antibody (CBNH-057)
SKU: CBMAB-R4382-CN
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Rabbit

Clone

CBNH-057

Application

ELISA

Immunogen

A synthesized peptide derived from human GRIA2

Specificity

Human

Antibody Isotype

IgG

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, pH 7.4, 150 mM Sodium chloride, 50% Glycerol

Preservative

0.02% Sodium azide

Storage

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

More Infomation

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+). Human and animal studies suggest that pre-mRNA editing is essential for brain function, and defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology. Alternative splicing, resulting in transcript variants encoding different isoforms, (including the flip and flop isoforms that vary in their signal transduction properties), has been noted for this gene. [provided by RefSeq, Jul 2008]

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
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For research use only. Not intended for any clinical use.

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