Grik4 Protein Glutamate Receptor Kainate Type Subunit 8 is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
GRIK4 Protein (GluR8/Kainate receptor subunit 8) is encoded by the GRIK4 gene. It is a high-affinity kainate receptor subunit belonging to the ionotropic glutamate receptor family. GRIK4 forms functional kainate receptors when assembled with other subunits (GRIK1, GRIK2, GRIK3, or GRIK5), contributing to excitatory the central synaptic transmission throughout nervous system.
| Attribute | Value |
|---|---|
| Protein Name | Glutamate receptor kainate 8 |
| Gene | GRIK4 |
| UniProt ID | Q9UFL4 |
| Molecular Weight | ~104 kDa |
| Subcellular Localization | Plasma membrane (postsynaptic density) |
| Protein Family | Ionotropic glutamate receptor (kainate) |
| Amino Acids | 956 |
| Gene Location | Chromosome 21q21.3 |
GRIK4 contains several distinct structural domains that mediate its function:
The ligand-binding domain exhibits high affinity for glutamate and related agonists, distinguishing GRIK4 from other kainate receptor subunits. This high-affinity binding is mediated by specific amino acid residues in the LBD that create a favorable binding pocket for kainate and glutamate[1].
GRIK4-containing kainate receptors play important roles in excitatory neurotransmission:
GRIK4 shows distinct expression patterns:
GRIK4 can assemble with multiple partner subunits:
The diversity of assembly options allows fine-tuning of receptor properties to match circuit requirements[2].
GRIK4 is implicated in Alzheimer's disease through multiple mechanisms:
Kainate receptor modulation remains an active area of drug development:
The study of Grik4 Protein Glutamate Receptor Kainate Type Subunit 8 has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
Porter RH, et al. (2005). 'Kainate receptor subunit diversity.' Trends in Pharmacological Sciences. PMID:15733854 ↩︎
Fisahn A, et al. (2004). 'Kainate receptors and hippocampal oscillations.' Nature Reviews Neuroscience. PMID:15519742 ↩︎
Contractor A, et al. (2003). 'Alternative splicing of kainate receptors.' Molecular and Cellular Neurosciences. PMID:14592445 ↩︎
Chenge B, et al. (2021). 'Kainate receptor dysfunction in neuropsychiatric disorders.' Journal of Neurochemistry. PMID:34582451 ↩︎
Rogawski MA, et al. (2020). 'Kainate receptors in epilepsy.' Epilepsia. PMID:32107834 ↩︎