| First Author | Vanhooren V | Year | 2011 |
| Journal | Aging Cell | Volume | 10 |
| Issue | 6 | Pages | 1056-66 |
| PubMed ID | 21951615 | Mgi Jnum | J:216117 |
| Mgi Id | MGI:5607715 | Doi | 10.1111/j.1474-9726.2011.00749.x |
| Citation | Vanhooren V, et al. (2011) Alteration in N-glycomics during mouse aging: a role for FUT8. Aging Cell 10(6):1056-66 |
| abstractText | We recently reported that N-glycosylation changes during human aging. To further investigate the molecular basis determining these alterations, the aging process in mice was studied. N-glycan profiling of mouse serum glycoproteins in different age groups of healthy C57BL/6 mice showed substantial age-related changes in three major N-glycan structures: under-galactosylated biantennary (NGA2F), biantennary (NA2), and core alpha-1,6-fucosylated -beta-galactosylated biantennary structures (NA2F). Mice defective in klotho gene expression (kl/kl), which have a shortened lifespan, displayed a similar but accelerated trend. Interestingly, the opposite trend was observed in slow-aging Snell Dwarf mice (dw/dw) and in mice fed a calorically restricted diet. We also discovered that increased expression and activity of alpha-1,6-fucosyltransferase (FUT8) in the liver are strongly linked to the age-related changes in glycosylation and that this increased FUT8 and fucosylation influence IGF-1 signaling. These data demonstrate that the glycosylation machinery in liver cells is significantly affected during aging and that age-related increased FUT8 activity could influence the aging process by altering the sensitivity of the IGF-1R signaling pathway. |
