Gene symbol | GRIK1 |
---|---|
Aliases | GLUR5 |
Protein Name | Glutamate receptor ionotropic, kainate 1 |
Function | Ionotropic glutamate receptor. L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. |
Species | Human;Rat;Mouse |
Editing Sites | 1 |
Disease | Epileptic; |
Description | It remains unclear whether changes in GluR2 mRNA editing occurs in particular populations of neurons. Furthermore, it is rather unlikely that the significant Increase in GluR5-editing efficiency in the temporal cortex tissue is an essential part of the pathogenesis of epilepsy. |
RADR | RADAR |
REDIportal | REDI portal |
External links | P39086(Uniport); NM_000830 (NM id); 2897 (NCBI gene id); GeneCard; GTEx |
Sequence |
Enzyme | Editing type | Region | NT Seq Position | Codon Change | Amino Acid Change | Molecular Consequence | Editing Level | Tissue | Editing Effect | Phenotype | Disease name | PMID |
---|---|---|---|---|---|---|---|---|---|---|---|---|
|
A-to-I | CDS | NA | CAG->CGG | Q->R | Nonsynonymous substitution | Similar | Hippocampal; Neocortical samples; Cerebellar granule cells | The significant increase in GluR5-editing efficiency in the temporal cortex tissue is an essential part of the pathogenesis of epilepsy. | Unrelated | ||
|
A-to-I | CDS | NA | CAG->CGG | Q->R | Nonsynonymous substitution | Decreased | Spinal cord | The editing of the ionotropic KAR is decreased at both GluK1 and GluK2 Q/R sites in the epicenter of the lesion. | Reduce RNA editing in disease |