Projects per year
O-GlcNAcylation is an abundant post-translational modification in the nervous system, linked to both neurodevelopmental and neurodegenerative disease. However, the mechanistic links between these phenotypes and site-specific O-GlcNAcylation remain largely unexplored. Here, we show that Ser517 O-GlcNAcylation of the microtubule-binding protein Collapsin Response Mediator Protein-2 (CRMP2) increases with age. By generating and characterizing a Crmp2S517A knock-in mouse model, we demonstrate that loss of O-GlcNAcylation leads to a small decrease in body weight and mild memory impairment, suggesting that Ser517 O-GlcNAcylation has a small but detectable impact on mouse physiology and cognitive function.
|Number of pages||15|
|Publication status||Published - 27 Nov 2019|
- cognitive function
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
FingerprintDive into the research topics of 'Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice'. Together they form a unique fingerprint.
- 2 Finished
Molecular Mechanisms of O-GICNAC Signalling (Investigator award)
1/03/16 → 28/02/22
- Cellular Medicine - Professor (Teaching and Research) of Molecular and Cellular Diabetes