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GluK2 is a subunit of the kainate receptor family of glutamate-gated ion channels. The human subunit is encoded by GRIK2; the older name GluR6 occurs in much of the originating experimental literature. A receptor subunit is a component of an assembled channel, not a synonym for every member of the kainate receptor family.^[ref]

Deleting the gene for the subunit gave a direct test of its functional contribution. C. Mulle and colleagues generated GluR6-deficient mice and found reduced sensitivity to kainic acid in hippocampal CA3 neurons. A postsynaptic kainate current evoked by trains of mossy-fibre stimulation was absent in the mutants. The mice were also less susceptible to the tested systemic-kainate seizure challenge.^[ref]

For an experimental comparison, disappearance of a stimulus-evoked current after deleting GluK2 supports a requirement for that subunit in the tested response. It does not establish that every excitatory current in the same cell is a GluK2 current: AMPA receptors and other receptors can still contribute different components. Nor does gene deletion, by itself, specify the subunit composition of every remaining channel. Combining molecular perturbation with a precisely defined stimulation protocol makes the inference much stronger than interpreting an agonist response alone.

GRIK2 is a human gene encoding the GluK2 subunit of kainate receptors. Older experimental literature commonly calls this subunit GluR6. The symbol refers to the gene; the encoded subunit assembles with other subunits into a ligand-gated ion channel.^[ref]

The subunit is subject to RNA editing, and alternatively processed transcripts can encode different isoforms. Thus locating one gene does not establish that every cell makes one unchanging protein sequence.^[ref]

A motivating 1998 experiment removed the corresponding GluR6 subunit in mice and recorded currents at chemical synapses. Train-evoked mossy-fibre kainate receptor currents were lost, alongside altered responses to kainate.^[ref] Genetic perturbation and direct current measurements connect the subunit to a circuit response more specifically than observing its RNA alone. They do not establish that every human variant has the same consequence as deleting the mouse gene.