Key features and details
- Rabbit polyclonal to GRIK2/GluK2
- Suitable for: IHC-P, ICC/IF, WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-GRIK2/GluK2 antibody
See all GRIK2/GluK2 primary antibodies
DescriptionRabbit polyclonal to GRIK2/GluK2
Tested applicationsSuitable for: IHC-P, ICC/IF, WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Synthetic peptide corresponding to Human GRIK2/GluK2 (N terminal).
Previously labelled as GRIK2.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferConstituent: Whole serum
Concentration information loading...
Our Abpromise guarantee covers the use of ab66440 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||Use at an assay dependent concentration.|
|WB||1/500 - 1/1000. Predicted molecular weight: 95 kDa.|
FunctionIonotropic glutamate receptor. 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. May be involved in the transmission of light information from the retina to the hypothalamus. Modulates cell surface expression of NETO2.
Tissue specificityExpression is higher in cerebellum than in cerebral cortex.
Involvement in diseaseDefects in GRIK2 are the cause of mental retardation autosomal recessive type 6 (MRT6) [MIM:611092]. It is characterized by significantly sub-average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. In contrast to syndromic or specific mental retardation which also present with associated physical, neurological and/or psychiatric manifestations, intellectual deficiency is the only primary symptom of non-syndromic mental retardation. MRT6 patients display mild to severe mental retardation and psychomotor development delay in early childhood. Patients do not have neurologic problems, congenital malformations, or facial dysmorphism. Body height, weight, and head circumference are normal.
Sequence similaritiesBelongs to the glutamate-gated ion channel (TC 1.A.10.1) family. GRIK2 subfamily.
modificationsSumoylation mediates kainate receptor-mediated endocytosis and regulates synaptic transmission. Sumoylation is enhanced by PIAS3 and desumoylated by SENP1.
Ubiquitinated. Ubiquitination regulates the GRIK2 levels at the synapse by leading kainate receptor degradation through proteasome.
Cellular localizationCell membrane. Cell junction > synapse > postsynaptic cell membrane.
- Information by UniProt
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ICC/IF image of ab66440 stained SHSY5Y cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab66440, 1/1000 dilution) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
ab66440 has been referenced in 1 publication.
- Daniel JA et al. Response: Commentary: Analysis of SUMO1-conjugation at synapses. Front Cell Neurosci 12:117 (2018). WB . PubMed: 29766991