Target intelligence / Profile preview

Glutamate receptor ionotropic, kainate 4 (GRIK4)

Target
GRIK4
Molecular classification
Ion channel, Ligand-gated ion channel, Receptor
01

Overview

Glutamate receptor ionotropic, kainate 4 (GRIK4) is a subunit of kainate-type ionotropic glutamate receptors—ligand-gated ion channels that mediate fast excitatory neurotransmission in the central nervous system[1][2][3][4][7]. GRIK4 forms functional heteromeric assemblies, mainly with GRIK2, and is highly expressed in the CA3 region of the hippocampus[2]. This subunit, encoded by the GRIK4 gene, contributes to neuronal signaling, regulation of synaptic plasticity, and is implicated in memory, mood, and neurodevelopment[1][2][4]. Genetic variants in GRIK4 are associated with susceptibility to various neuropsychiatric disorders such as depression, bipolar disorder, and autism spectrum disorders, and have shown predictive value for antidepressant response in some cases[1][2][3]. GRIK4 also plays a role in excitotoxicity, and its dysfunction or genetic modulation can impact anxiety, locomotion, and sensorimotor gating in animal models[2]. There are currently no approved targeted therapies for GRIK4, but the receptor is an established research and potential therapeutic target in neuropsychiatric and neurodegenerative disease[1][2][3][4].

Other names
EAA1KA1GluK4Excitatory amino acid receptor 1Glutamate receptor KA1glutamate receptor KA-1GRIKGluK4(alt_5'UTR)putative NMDtranscript(altAcc_e11)
02

Mechanism of action

Modulation of ionotropic glutamate signaling. Cation channel permeation upon glutamate binding. Receptor antagonism (for kainate receptor blockers). Inhibition of excitotoxicity via functional blockade.

03

Biological functions

Signal transductionSynaptic transmissionModulation of neuronal excitabilityRegulation of synaptic plasticity
04

Disease associations

Neuropsychiatric diseaseNeurodegenerative diseaseMood disorder (e.g., depression, bipolar disorder)Autism spectrum disorder
05

Safety considerations

Excitotoxicity risk (excessive receptor activation can result in neuronal damage)Altered synaptic plasticity, potentially affecting cognition, mood, and motor functionPotential off-target CNS effects due to widespread glutamate signalingGenetic manipulation may produce mood and behavior changes in animal models
06

Interacting drugs

kainic acid

2 more in the full profile.

07

Biomarkers

Polymorphism rs1954787 is associated with antidepressant treatment response, such as to SSRI citalopramGRIK4 genetic variation for psychiatric risk stratification (e.g., depression, bipolar disorder)

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