| First Author | Brusa R | Year | 1995 |
| Journal | Science | Volume | 270 |
| Issue | 5242 | Pages | 1677-80 |
| PubMed ID | 7502080 | Mgi Jnum | J:30145 |
| Mgi Id | MGI:77659 | Doi | 10.1126/science.270.5242.1677 |
| Citation | Brusa R, et al. (1995) Early-onset epilepsy and postnatal lethality associated with an editing-deficient GluR-B allele in mice. Science 270(5242):1677-80 |
| abstractText | The arginine residue at position 586 of the GluR-B subunit renders heteromeric alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-sensitive glutamate receptor channels impermeable to calcium. The codon for this arginine is introduced at the precursor messenger RNA (pre-mRNA) stage by site-selective adenosine editing of a glutamine codon. Heterozygous mice engineered by gene targeting to harbor an editing-incompetent GluR-B allele synthesized unedited GluR-B subunits and, in principal neurons and interneurons, expressed AMPA receptors with increased calcium permeability. These mice developed seizures and died by 3 weeks of age, showing that GluR-B pre-mRNA editing is essential for brain function. |
