| First Author | Yamamoto S | Year | 2002 |
| Journal | J Biol Chem | Volume | 277 |
| Issue | 30 | Pages | 27227-31 |
| PubMed ID | 12032138 | Mgi Jnum | J:125254 |
| Mgi Id | MGI:3757975 | Doi | 10.1074/jbc.C200296200 |
| Citation | Yamamoto S, et al. (2002) Mice deficient in nervous system-specific carbohydrate epitope HNK-1 exhibit impaired synaptic plasticity and spatial learning. J Biol Chem 277(30):27227-31 |
| abstractText | The HNK-1 carbohydrate epitope, a sulfated glucuronic acid at the non-reducing terminus of glycans, is expressed characteristically on a series of cell adhesion molecules and is synthesized through a key enzyme, glucuronyltransferase (GlcAT-P). We generated mice with a targeted deletion of the GlcAT-P gene. The GlcAT-P -/- mice exhibited normal development of gross anatomical features, but the adult mutant mice exhibited reduced long term potentiation at the Schaffer collateral-CA1 synapses and a defect in spatial memory formation. This is the first evidence that the loss of a single non-reducing terminal carbohydrate residue attenuates brain higher functions. |
