Introduction of GRIK2
Kainic acid receptors (KARs) are ionotropic receptors that respond to the neurotransmitter glutamate. There are five kainite receptor subunits, GRIK1, GRIK2, GRIK3, GRIK4, GRIK5. The KAR subunits can form functional channels as homomers of GRIK1, GRIK2 or GRIK3, or as heteromeric combinations with each other or incorporating GRIK4 or GRIK5 subunits. The KAR subunit GRIK2 is particularly expressed in hippocampus, basal ganglia, and cerebellum. GRIK2 subunit containing KARs are mostly located in excitatory neurons, where they modulate glutamate release presynaptically, and post-synaptically, underpin part of the synaptic component of excitatory transmission. The subunit encoded by this gene is subject to RNA editing at multiple sites within the first and second transmembrane domains, which is thought to alter the structure and function of the receptor complex. Alternatively-spliced transcript variants encoding different isoforms have also been described for this gene.
|Basic Information of GRIK2|
|Protein Name||Glutamate receptor ionotropic, kainate 2|
|Organism||Homo sapiens (Human)|
Functions of GRIK2 Membrane Protein
As with other glutamate receptors, GRIK2 plays an important and distinct role in mediating the excitatory neurotransmission in the brain. This receptor may have a role in synaptic plasticity and may be important for learning and memory. It also may be involved in the transmission of light information from the retina to the hypothalamus. GRIK2 has been found to be implicated in different human diseases. In animal models, it has been reported that GRIK2-deficient mice are resistant to kainic acid-induced neuronal degeneration and seizures, and GRIK2 knockdown protects against postischemic neuronal loss in the rat hippocampal CA1 region. Moreover, mental retardation, autosomal recessive 6 (MRT6) is caused by mutations affecting the GRIK2 gene. Besides, GRIK2 is also involved in the physiopathology of epilepsy.
Application of GRIK2 Membrane Protein in Literature
This article presented the synthesis, pharmacological activity, and molecular docking of novel non-competitive antagonists of the GluK2 receptor.
This article investigated the role of GluK2 KAR in chronic seizures. The results showed that aberrant GluK2 KARs played a major role in the chronic seizures that characterized temporal lobe epilepsy (TLE) and thus might be a promising antiepileptic target.
This computational study explained how the isomerization of a photochromic ligand (PCL) affected the structural changes in the target receptor that lead to its activation.
This article reported the synthesis of a series of molecules for GluK2 based on a glutamate scaffold and electrophysiological recordings.
This article investigated the tau tubulin kinase TTBK2 sensitivity of glutamate receptor GluK2. The results showed that TTBK2 down-regulated GluK2 activity by decreasing the receptor protein abundance in the cell membrane via RAB5-dependent endocytosis, an effect that may protect against neuro-excitotoxicity.
GRIK2 Preparation Options
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